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72<div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/virus-packaging/aav-packaging" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Adeno-associated Virus (AAV) Packaging</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/virus-packaging/adenovirus-packaging" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Adenovirus Packaging</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/virus-packaging/lentivirus-packaging" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Lentivirus Packaging</span><!--]--></a></div><!----></div><!--]--></div></div><div class="_menu_1epgt_31 _menu2_1epgt_200 t-delay"><div class="_name_1epgt_58 _childrens_1epgt_188"><!--[--><a href="/custom-cell-line-models" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Custom Cell Line Services</span><!--]--></a><svg class="ui-icon _icon_1epgt_169" aria-hidden="true"><use xlink:href="#icon-add"></use></svg><!--]--></div><div class="overflow-hidden" style="display:none;"><!--[--><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/custom-cell-line-models/ipsc" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Induced Pluripotent Stem Cells (iPSCs)</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/custom-cell-line-models/knockout-cell-lines" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Knockout Cell Lines</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/custom-cell-line-models/knockin-cell-lines" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Knockin Cell Lines</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/custom-cell-line-models/overexpression-cell-lines" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Overexpression Cell Lines</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/custom-cell-line-models/point-mutation-cell-lines" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Point Mutation Cell Lines</span><!--]--></a></div><!----></div><!--]--></div></div><div class="_menu_1epgt_31 _menu2_1epgt_200 t-delay"><div class="_name_1epgt_58 _childrens_1epgt_188"><!--[--><a href="/mouse-model-lifecycle" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Breeding & Supporting Services</span><!--]--></a><svg class="ui-icon _icon_1epgt_169" aria-hidden="true"><use xlink:href="#icon-add"></use></svg><!--]--></div><div class="overflow-hidden" style="display:none;"><!--[--><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/mouse-model-lifecycle/bac-modification" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>BAC Modification</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/mouse-model-lifecycle/breeding" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Breeding Services</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/mouse-model-lifecycle/cryopreservation-recovery" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Cryopreservation & Recovery</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/mouse-model-lifecycle/phenotyping" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Phenotyping Services</span><!--]--></a></div><!----></div><!--]--></div></div><!--]--></div></div>
72<div class="_menu_1epgt_31 _menu1_1epgt_177 t-delay"><div class="_name_1epgt_58 _childrens_1epgt_188"><!--[--><div data-ui-route class="_context_1epgt_1 block leading-[48rem] truncate"><!--[--><span>Preclinical Solutions</span><!--]--></div><svg class="ui-icon _icon_1epgt_169" aria-hidden="true"><use xlink:href="#icon-add"></use></svg><!--]--></div><div class="overflow-hidden" style="display:none;"><!--[--><div class="_menu_1epgt_31 _menu2_1epgt_200 t-delay"><div class="_name_1epgt_58 _childrens_1epgt_188"><!--[--><a href="/cro-services/antibody-therapy" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Antibody Discovery Platform</span><!--]--></a><svg class="ui-icon _icon_1epgt_169" aria-hidden="true"><use xlink:href="#icon-add"></use></svg><!--]--></div><div class="overflow-hidden" style="display:none;"><!--[--><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/cro-services/antibody-therapy/monoclonal-antibody-mouse-platform" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>HUGO-Mab™</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/cro-services/antibody-therapy/hugo-light-bispecific-antibody-discovery-mouse" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>HUGO-Light™</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/cro-services/hugo-nano-antibody-discovery" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>HUGO-Nano™</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/cro-services/antibody-therapy/hugo-ab-eko-target-knockout-antibody-discovery" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>HUGO-Ab-eKO™</span><!--]--></a></div><!----></div><!--]--></div></div><div class="_menu_1epgt_31 _menu2_1epgt_200 t-delay"><div class="_name_1epgt_58 _childrens_1epgt_188"><!--[--><a href="/cro-services" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Therapeutic Area</span><!--]--></a><svg class="ui-icon _icon_1epgt_169" aria-hidden="true"><use xlink:href="#icon-add"></use></svg><!--]--></div><div class="overflow-hidden" style="display:none;"><!--[--><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58 _childrens_1epgt_188"><!--[--><a href="/cro-services/neuroscience" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Neurology</span><!--]--></a><svg class="ui-icon _icon_1epgt_169" aria-hidden="true"><use xlink:href="#icon-add"></use></svg><!--]--></div><div class="overflow-hidden" style="display:none;"><!--[--><div class="_menu_1epgt_31 _menu4_1epgt_213"><div class="_name_1epgt_58"><a href="/cro-services/neuroscience/alzheimers-disease" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Alzheimer's Disease (AD)</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu4_1epgt_213"><div class="_name_1epgt_58"><a href="/cro-services/neuroscience/parkinsons-disease" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Parkinson's Disease (PD)</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu4_1epgt_213"><div class="_name_1epgt_58"><a href="/cro-services/neuroscience/huntingtons-disease" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Huntington's Disease (HD)</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu4_1epgt_213"><div class="_name_1epgt_58"><a href="/cro-services/neuroscience/blood-brain-barrier" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Blood Brain Barrier (BBB)</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu4_1epgt_213"><div class="_name_1epgt_58"><a href="/cro-services/neuroscience/neuropathic-pain" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Neuropathic Pain</span><!--]--></a></div><!----></div><!--]--></div></div>
72<div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58 _childrens_1epgt_188"><!--[--><a href="/cro-services/metabolic-diseases" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Metabolic</span><!--]--></a><svg class="ui-icon _icon_1epgt_169" aria-hidden="true"><use xlink:href="#icon-add"></use></svg><!--]--></div><div class="overflow-hidden" style="display:none;"><!--[--><div class="_menu_1epgt_31 _menu4_1epgt_213"><div class="_name_1epgt_58"><a href="/cro-services/metabolic-diseases/anti-obesity" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Obesity</span><!--]--></a></div><!----></div><!--]--></div></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/cro-services/cardiovascular-diseases" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Cardiovascular</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58 _childrens_1epgt_188"><!--[--><a href="/cro-services/ophthalmology" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Ophthalmology</span><!--]--></a><svg class="ui-icon _icon_1epgt_169" aria-hidden="true"><use xlink:href="#icon-add"></use></svg><!--]--></div><div class="overflow-hidden" style="display:none;"><!--[--><div class="_menu_1epgt_31 _menu4_1epgt_213"><div class="_name_1epgt_58"><a href="/cro-services/ophthalmology/glaucoma" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Glaucoma</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu4_1epgt_213"><div class="_name_1epgt_58"><a href="/cro-services/ophthalmology/age-related-macular-degeneration" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Age-Related Macular Degeneration (AMD)</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu4_1epgt_213"><div class="_name_1epgt_58"><a href="/cro-services/retinal-disease-models" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Retinal-related diseases</span><!--]--></a></div><!----></div><!--]--></div></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58 _childrens_1epgt_188"><!--[--><a href="/cro-services/oncology" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Oncology</span><!--]--></a><svg class="ui-icon _icon_1epgt_169" aria-hidden="true"><use xlink:href="#icon-add"></use></svg><!--]--></div><div class="overflow-hidden" style="display:none;"><!--[--><div class="_menu_1epgt_31 _menu4_1epgt_213"><div class="_name_1epgt_58"><a href="/cro-services/oncology/pbmc-nkg-mouse-model" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>PBMC Humanized Mouse Model</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu4_1epgt_213"><div class="_name_1epgt_58"><a href="/cro-services/oncology/hsc-nkg-mouse-model" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Human Immune System (HIS) Mouse Model</span><!--]--></a></div><!----></div><!--]--></div></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58 _childrens_1epgt_188"><!--[--><a href="/cro-services/autoimmunity-inflammation" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Immunology & Inflammation</span><!--]--></a><svg class="ui-icon _icon_1epgt_169" aria-hidden="true"><use xlink:href="#icon-add"></use></svg><!--]--></div><div class="overflow-hidden" style="display:none;"><!--[--><div class="_menu_1epgt_31 _menu4_1epgt_213"><div class="_name_1epgt_58"><a href="/cro-services/autoimmunity-inflammation/asthma" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Asthma</span><!--]--></a></div><!----></div><!--]--></div></div><!--]--></div></div><div class="_menu_1epgt_31 _menu2_1epgt_200 t-delay"><div class="_name_1epgt_58 _childrens_1epgt_188"><!--[--><a href="/cro-services" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Drug Classification</span><!--]--></a><svg class="ui-icon _icon_1epgt_169" aria-hidden="true"><use xlink:href="#icon-add"></use></svg><!--]--></div><div class="overflow-hidden" style="display:none;"><!--[-->
72<div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58 _childrens_1epgt_188"><!--[--><div data-ui-route class="_context_1epgt_1 block leading-[48rem] truncate"><!--[--><span>Therapeutic Antibody Drugs</span><!--]--></div><svg class="ui-icon _icon_1epgt_169" aria-hidden="true"><use xlink:href="#icon-add"></use></svg><!--]--></div><div class="overflow-hidden" style="display:none;"><!--[--><div class="_menu_1epgt_31 _menu4_1epgt_213"><div class="_name_1epgt_58"><a href="/cro-services/monoclonal-antibody-discovery" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Monoclonal Antibodies (mAb)</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu4_1epgt_213"><div class="_name_1epgt_58"><a href="/cro-services/bispecific-multispecific-antibody-discovery-development" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Bispecific Antibodies (BsAb)</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu4_1epgt_213"><div class="_name_1epgt_58"><a href="/cro-services/adc-aoc" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>ADC/AOC</span><!--]--></a></div><!----></div><!--]--></div></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/cro-services/ai-powered-aav-discovery" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>AI-Powered AAV Discovery</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/cro-services/cell-immunotherapy" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Cell Immunotherapy</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/cro-services/gene-therapy" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Gene Therapy</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/cro-services/oligonucleotide-therapy" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Oligonucleotide Therapy</span><!--]--></a></div><!----></div><!--]--></div></div><div class="_menu_1epgt_31 _menu2_1epgt_200 t-delay"><div class="_name_1epgt_58 _childrens_1epgt_188"><!--[--><a href="/antibody-library" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Fully Human Antibody Library</span><!--]--></a><svg class="ui-icon _icon_1epgt_169" aria-hidden="true"><use xlink:href="#icon-add"></use></svg><!--]--></div><div class="overflow-hidden" style="display:none;"><!--[--><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/antibody-library/neuroscience-neuromuscular-antibody-library" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Neurology Antibodies</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/antibody-library/metabolic-cardiovascular-antibody-library" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Metabolic & Cardiovascular Antibodies</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/antibody-library/ophthalmology-antibody-library" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Ophthalmology Antibodies</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/antibody-library/oncology-antibody-library" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Oncology Antibodies</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="/antibody-library/immunology-inflammation-antibody-library" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Immunology & Inflammation Antibodies</span><!--]--></a></div><!----></div><!--]--></div></div><!--]--></div></div>
72<div class="_menu_1epgt_31 _menu1_1epgt_177 t-delay"><div class="_name_1epgt_58 _childrens_1epgt_188"><!--[--><div data-ui-route class="_context_1epgt_1 block leading-[48rem] truncate"><!--[--><span>Resources</span><!--]--></div><svg class="ui-icon _icon_1epgt_169" aria-hidden="true"><use xlink:href="#icon-add"></use></svg><!--]--></div><div class="overflow-hidden" style="display:none;"><!--[--><div class="_menu_1epgt_31 _menu2_1epgt_200 t-delay"><div class="_name_1epgt_58"><a href="/news" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>News</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu2_1epgt_200 t-delay"><div class="_name_1epgt_58"><a href="/cyagen-lab-notes" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Blogs & Insight</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu2_1epgt_200 t-delay"><div class="_name_1epgt_58"><a href="/campaigns" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Promotion</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu2_1epgt_200 t-delay"><div class="_name_1epgt_58"><a href="/events" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Events & Webinars</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu2_1epgt_200 t-delay"><div class="_name_1epgt_58 _childrens_1epgt_188"><!--[--><div data-ui-route class="_context_1epgt_1 block leading-[48rem] truncate"><!--[--><span>Databases</span><!--]--></div><svg class="ui-icon _icon_1epgt_169" aria-hidden="true"><use xlink:href="#icon-add"></use></svg><!--]--></div><div class="overflow-hidden" style="display:none;"><!--[--><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="https://abseek.icyagen.com/" data-ui-route class="_context_1epgt_1 block leading-[48rem] truncate"><!--[--><span>AbSeek</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="https://rddc.tsinghua-gd.org/zh" data-ui-route class="_context_1epgt_1 block leading-[48rem] truncate"><!--[--><span>Rare Disease Data Center</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="https://www.alphaknockout.com/" data-ui-route class="_context_1epgt_1 block leading-[48rem] truncate"><!--[--><span>Cell iGeneEditor™ System</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu3_1epgt_208 t-delay"><div class="_name_1epgt_58"><a href="https://www.icyagen.com/" data-ui-route class="_context_1epgt_1 block leading-[48rem] truncate"><!--[--><span>iCyagen</span><!--]--></a></div><!----></div><!--]--></div></div><div class="_menu_1epgt_31 _menu2_1epgt_200 t-delay"><div class="_name_1epgt_58"><a href="/reference/model-citations" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Citations</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu2_1epgt_200 t-delay"><div class="_name_1epgt_58"><a href="/resource-repository" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Resource Vault</span><!--]--></a></div><!----></div><div class="_menu_1epgt_31 _menu2_1epgt_200 t-delay"><div class="_name_1epgt_58"><a href="https://www.oricellbio.com/" data-ui-route class="_context_1epgt_1 block leading-[48rem] truncate"><!--[--><span>OriCell</span><!--]--></a></div><!----></div><!--]--></div></div><div class="_menu_1epgt_31 _menu1_1epgt_177 t-delay"><div class="_name_1epgt_58 _childrens_1epgt_188"><!--[--><div data-ui-route class="_context_1epgt_1 block leading-[48rem] truncate"><!--[--><span>About Us</span><!--]--></div><svg class="ui-icon _icon_1epgt_169" aria-hidden="true"><use xlink:href="#icon-add"></use></svg><!--]--></div><div class="overflow-hidden" style="display:none;"><!--[--><div class="_menu_1epgt_31 _menu2_1epgt_200 t-delay"><div class="_name_1epgt_58"><a href="/mice-quality-program/animal-walfare" class="_context_1epgt_1 block leading-[48rem] truncate" data-ui-route><!--[--><span>Animal Health & Welfare</span><!--]--></a></div><!----></div>
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IL-17A is primarily produced by Th17 cells and can also be produced by other immune cells under certain conditions, including CD8+ T cells, γδT cells, natural killer T (NKT) cells, monocytes, neutrophils, and microglia <sup>[1]</sup>. IL-17A mediates downstream pathways that induce the production of inflammatory molecules, chemokines, antimicrobial peptides, and remodeling proteins, which have important effects on host defense, cell transport, immune regulation, and tissue repair, especially in inducing innate immune defense. In healthy skin, commensal microorganisms induce the production of IL-17A to provide antifungal protection. When the skin barrier is damaged, IL-17A promotes epithelial cell proliferation and can clear pathogenic factors, promoting tissue repair and wound healing <sup>[2]</sup>. IL-17A usually protects the body when it is acutely injured, but when a wound requires long-term healing and becomes a chronic injury, the role of IL-17A may transform into wound erosion or excessive proliferation, ultimately leading to loss of function <sup>[3]</sup>. \nIL-17A plays a key role in various infectious diseases, inflammations, autoimmune diseases, and cancers. Its high expression level is associated with chronic inflammatory diseases such as rheumatoid arthritis, psoriasis, and multiple sclerosis. Lung injury caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is largely the result of the promotion of inflammatory reactions by cytokines such as IL-17A. Dysregulation of IL-17 signaling promotes pathogenic inflammation. IL-17A has a pathogenic role in mediating the important inflammatory pathway of psoriasis. The IL-23/Th17/IL-17A pathway is a key link in its pathogenesis, and inhibiting the expression of IL-17A can effectively alleviate psoriasis <sup>[4]</sup>. IL-17A is also associated with the course of ankylosing spondylitis (AS), and IL-17A inhibitors can effectively treat AS <sup>[5]</sup>
97. In addition, studies have shown that IL-17A is involved in the pathogenesis of neurodegenerative diseases in the central nervous system, and its expression level is related to the severity and progression of the disease <sup>[3]</sup>.\nhuIL17A mice are humanized mouse models that express human IL-17A protein. They were constructed by using gene editing technology to replace the sequence encoding the endogenous extracellular domain of the mouse Il17a gene with the corresponding sequence from the human IL17A gene while retaining the mouse signal peptide. This strain can be used for mechanism research and preclinical evaluation of therapeutic drugs for various chronic inflammatory diseases such as rheumatoid arthritis, psoriasis, and multiple sclerosis. The homozygotes are viable and fertile.","label":"Animal Models","link":"mouseatlas/C001510","tags":[],"title":"C57BL/6NCya-<i>Il17a<sup>em1(hIL17A)</sup></i>/Cya"},{"description":"The huTFRC/huSNCA(3'UTR)/hutau mouse is a triple-gene humanized model generated by crossing the huTFRC mouse (Catalog No.: <a href=\"https://www.cyagen.com/mouseatlas/C001860\" style=\"color: var(--uicolor-main-color);text-decoration: underline;text-underline-offset: 4px;\" target=\"_blank\">C001860</a>), the huSNCA(2) mouse (Catalog No.: <a href=\"https://www.cyagen.com/mouseatlas/C001698\" style=\"color: var(--uicolor-main-color);text-decoration: underline;text-underline-offset: 4px;\" target=\"_blank\">C001698</a>), and the huTau(MAPT) mouse (Catalog No.: <a href=\"https://www.cyagen.com/mouseatlas/C001410\" style=\"color: var(--uicolor-main-color);text-decoration: underline;text-underline-offset: 4px;\" target=\"_blank\">C001410</a>). This model can be used for evaluating TFRC-mediated blood-brain barrier (BBB) delivery strategies, as well as for the screening, pharmacodynamic evaluation, safety assessment, and mechanism-of-action studies of TFRC/SNCA/MAPT-targeted therapeutics. It provides a valuable preclinical platform for developing innovative therapies for Alzheimer's disease (AD), Parkinson's disease (PD), and other neurodegenerative diseases.","label":"Animal Models","link":"mouseatlas/C002100","tags":[],"title":"C57BL/6J;6NCya-<i>Tfrc<sup>tm2(hTFRC)</sup>Snca<sup>tm2(hSNCA)</sup>Mapt<sup>tm1(hMAPT)</sup></i>/Cya"},{"description":"Programmed cell death protein 1 (PDCD1/PD-1) is a member of the B7-CD28 family of costimulatory receptor proteins. It is expressed on activated T cells and functions as an immunosuppressive receptor involved in regulating the function of effector T cells, including CD8<sup>+</sup> T cells, and promoting the differentiation of CD4<sup>+</sup> T cells into regulatory T cells. PD-1 is expressed in various tumors and plays an important role in antitumor immunity. In addition, PD-1 is involved in immune tolerance and suppresses antitumor and antimicrobial immune responses<sup> [1]</sup>.\nPDL1, also known as programmed cell death 1 ligand 1 (PD-L1), cluster of differentiation 274 (CD274), or B7 homolog 1 (B7-H1), encodes an immunosuppressive receptor ligand mainly expressed by hematopoietic and non-hematopoietic cells, including T cells, B cells, and various tumor cells<sup> [2]</sup>. PD-L1 is a type I transmembrane protein containing immunoglobulin V-like (IgV) and C-like (IgC) domains. PD-L1 interacts with the PD-1 receptor expressed on T cells, thereby inhibiting T cell activation and effector function. This interaction prevents excessive immune responses against normal tissues but can also be exploited by tumor cells to evade immune surveillance. Monoclonal antibodies targeting PD-L1 can disrupt the interaction between PD-1 and PD-L1, reverse PD-1/PD-L1-mediated immune suppression, reactivate T cells, and initiate antitumor immune responses<sup> [3]</sup>.\nThe CD19 gene encodes a member of the immunoglobulin superfamily and serves as a key co-receptor in the B cell receptor (BCR) signaling pathway, playing an essential role in B cell development, activation, and differentiation. CD19 is a pan-B cell marker that is specifically expressed in the B cell lineage and remains stably expressed throughout B cell development, from pre-B cells to mature B cells and memory B cells. CD19 acts as a positive regulator of BCR signaling. The CD19 protein forms a B cell-specific signaling complex with CD21 (complement receptor type 2), CD81 (tetraspanin), and CD225 (Leu13), which lowers the threshold for antigen-induced B cell activation<sup> [4]</sup>.\nThe huPD-1/hPD-L1/huCD19 mouse is a triple-gene humanized model generated by crossing the hPDL1-V(2) mouse (Catalog No.: <a href=\"https://www.cyagen.com/mouseatlas/C001235\" style=\"color: var(--uicolor-main-color);text-decoration: underline;text-underline-offset: 4px;\" target=\"_blank\">C001235</a>), the huPD-1 mouse (Catalog No.: <a href=\"https://www.cyagen.com/mouseatlas/C001524\" style=\"color: var(--uicolor-main-color);text-decoration: underline;text-underline-offset: 4px;\" target=\"_blank\">C001524</a>), and the huCD19 mouse (Catalog No.: <a href=\"https://www.cyagen.com/mouseatlas/C001731\" style=\"color: var(--uicolor-main-color);text-decoration: underline;text-underline-offset: 4px;\" target=\"_blank\">C001731</a>). This model can be used for pharmacodynamic evaluation, mechanism of action studies, and combination therapeutic strategy development of anti-CD19 therapeutics and PD-1/PD-L1 immune checkpoint inhibitors. It supports the evaluation of combination therapies involving anti-CD19 CAR-T cells, bispecific antibodies, and immune checkpoint inhibitors, as well as studies of B cell–T cell interactions and tumor immune microenvironment mechanisms. This model provides a preclinical research platform for developing innovative immunotherapies for B-cell malignancies, including acute lymphoblastic leukemia (ALL) and non-Hodgkin lymphoma (NHL).","label":"Animal Models","link":"mouseatlas/C002087","tags":[],"title":"C57BL/6J;6NCya-<i>Pdcd1<sup>em1(hPDCD1)</sup>Cd274<sup>em1(hCD274)</sup>Cd19<sup>em3(hCD19)</sup></i>/Cya"},{"description":"Growth differentiation factor 8 (GDF8) is a key negative regulator of skeletal muscle growth that inhibits the proliferation and differentiation of muscle cells and maintains muscle mass homeostasis<sup> [1-4]</sup>. Activin receptor-like kinase 7 (ALK7, ACVR1C) is a type I receptor of the transforming growth factor-β (TGF-β) superfamily. It is widely expressed in adipose tissue and metabolically active organs and participates in the regulation of adipogenesis, energy metabolism, and glucose homeostasis<sup> [5-6]</sup>. Inhibin beta E subunit (INHBE) is a liver-specific member of the TGF-β superfamily. The Activin E encoded by INHBE functions as a hepatokine that plays an important role in maintaining metabolic homeostasis by regulating lipid storage, adipose tissue function, and systemic energy metabolism<sup> [7]</sup>. Recent studies have further demonstrated that the INHBE-ALK7 signaling axis participates in the metabolic regulation between the liver and adipose tissue, and its dysregulation is closely associated with metabolic diseases, including obesity, type 2 diabetes (T2D), and metabolic dysfunction-associated steatotic liver disease (MASLD)<sup> [8]</sup>. Meanwhile, GDF8-mediated regulation of skeletal muscle mass is extensively interconnected with adipose and hepatic metabolism<sup> [9-10]</sup>. GDF8, INHBE, and ALK7 each participate in the metabolic regulation among these tissues and collectively influence whole-body energy homeostasis, fat distribution, and glucose metabolism, providing new insights into combination intervention strategies for promoting muscle growth, reducing adiposity, and improving metabolic health.\nThe huGDF8/huALK7/huINHBE mouse is a triple-gene humanized model that can be generated by intercrossing the huMSTN(GD
97F8) mouse (Catalog No.: <a href=\"https://www.cyagen.com/mouseatlas/C001636\" style=\"color: var(--uicolor-main-color);text-decoration: underline;text-underline-offset: 4px;\" target=\"_blank\">C001636</a>), the huALK7(ACVR1C) mice (Catalog No.: <a href=\"https://www.cyagen.com/mouseatlas/C001911\" style=\"color: var(--uicolor-main-color);text-decoration: underline;text-underline-offset: 4px;\" target=\"_blank\">C001911</a>) and the huINHBE mice (Catalog No.: <a href=\"https://www.cyagen.com/mouseatlas/C001533\" style=\"color: var(--uicolor-main-color);text-decoration: underline;text-underline-offset: 4px;\" target=\"_blank\">C001533</a>). This model simultaneously carries the humanized GDF8, ACVR1C, and INHBE genes and can be used for the screening, pharmacodynamic evaluation, safety assessment, and mechanism of action studies of therapeutics targeting GDF8, ACVR1C, and INHBE, as well as studies on body composition remodeling, regulation of the muscle-adipose-liver metabolic axis, and energy metabolic reprogramming. It also serves as a preclinical research platform for developing combination therapeutic strategies for promoting muscle growth, reducing adiposity, and improving metabolic health, as well as innovative therapies for metabolic diseases, including obesity, type 2 diabetes (T2D), and metabolic dysfunction-associated steatotic liver disease (MASLD).","label":"Animal Models","link":"mouseatlas/C002082","tags":[],"title":"C57BL/6NCya-<i>Mstn<sup>em1(hMSTN)</sup>Acvr1c<sup>tm1(hACVR1C)</sup>Inhbe<sup>tm1(hINHBE)</sup></i>/Cya"},{"description":"The huIL4/huIL4R/hOSMR mouse is a triple-gene humanized model obtained by crossing the huIL4/huIL4RA mouse (Catalog No.: <a href=\"https://www.cyagen.com/mouseatlas/C001834\" style=\"color: var(--uicolor-main-color);text-decoration: underline;text-underline-offset: 4px;\" target=\"_blank\">C001834</a>) with the hOSMR mouse (Catalog No.: <a href=\"https://www.cyagen.com/mouseatlas/C001841\" style=\"color: var(--uicolor-main-color);text-decoration: underline;text-underline-offset: 4px;\" target=\"_blank\">C001841</a>). The huIL4/huIL4R/hOSMR mouse is a multi-target humanized model that integrates Th2-type immune-inflammatory regulation with tissue inflammatory response regulation. Co-expressing humanized IL4, IL4R, and OSMR genes, this model can be utilized for the screening, pharmacodynamic evaluation, safety assessment, and mechanism of action studies of multi-target therapeutics targeting IL4, IL4R, and OSMR. It serves as an ideal preclinical research platform for developing innovative therapies for atopic dermatitis (AD) and other Th2-mediated inflammatory diseases.","label":"Animal Models","link":"mouseatlas/C002072","tags":[],"title":"C57BL/6NCya-<i>Il4<sup>em1(hIL4)</sup>Il4ra<sup>em1(hIL4R)</sup>Osmr<sup>tm1(hOSMR)</sup></i>/Cya"},{"description":"The huIL4/huIL4R/huTSLP/hTSLPR mice are a quadruple-gene humanized model obtained by mating huIL4/huIL4R mice (catalog number: <a href=\"https://www.cyagen.com/mouseatlas/C001834\" style=\"color: var(--uicolor-main-color);text-decoration: underline;text-underline-offset: 4px;\" target=\"_blank\">C001834</a>), huTSLP mice (catalog number: <a href=\"https://www.cyagen.com/mouseatlas/C001809\" style=\"color: var(--uicolor-main-color);text-decoration: underline;text-underline-offset: 4px;\" target=\"_blank\">C001809</a>), and hTSLPR mice (catalog number: <a href=\"https://www.cyagen.com/mouseatlas/C001942\" style=\"color: var(--uicolor-main-color);text-decoration: underline;text-underline-offset: 4px;\" target=\"_blank\">C001942</a>). This model is a valuable tool for studying allergic diseases (such as asthma and atopic dermatitis), Th2 immune responses, parasitic infections, tumor immunology, and chronic inflammation. In addition, this model also provides a powerful preclinical research platform for evaluating the efficacy and mechanism of therapeutic drugs targeting IL4/IL4R/TSLP/TSLPR.","label":"Animal Models","link":"mouseatlas/C001996","tags":[],"title":"C57BL/6NCya-<i>Il4<sup>em1(hIL4)</sup>Il4ra<sup>em1(hIL4R)</sup>Tslp<sup>em1(hTSLP)</sup>Crlf2<sup>tm1(hCRLF2)</sup></i>/Cya"},{"description":"The IL23A gene encodes the p19 subunit, a component of interleukin-23 (IL-23), which forms a heterodimer with the p40 subunit (encoded by IL12B) to generate the functional IL-23 cytokine <sup>[1]</sup>. Primarily expressed by activated dendritic cells, macrophages, and monocytes, IL-23 signals through the IL-23 receptor (IL-23R) complex, activating the JAK-STAT pathway to promote Th17 cell differentiation and maintain IL-17 production. This process drives inflammatory responses and mucosal immunity against extracellular pathogens <sup>[1-2]</sup>. Genetic polymorphisms within IL23A are strongly associated with autoimmune and inflammatory diseases, including psoriasis, Crohn's disease, and inflammatory bowel disease, due to dysregulated Th17 activity and chronic inflammation <sup>[1-2]</sup>. Monoclonal antibodies targeting IL-23, such as risankizumab and guselkumab, selectively block the p19 subunit, demonstrating therapeutic efficacy in psoriasis and inflammatory bowel diseases by suppressing pathogenic IL-17/Th17 pathways <sup>[3]</sup>. Also, monoclonal antibodies targeting IL-12B, such as ustekinumab, are clinically utilized for the treatment of moderate to severe psoriasis and Crohn's disease <sup>[4]</sup>. While IL-23 plays a role in protective immunity, its overactivation contributes to tissue damage in autoimmune settings, highlighting its dual function in immune regulation and disease pathogenesis <sup>[1-5]</sup>.\nTNF-like ligand 1A (TL1A), also known as TNF superfamily member 15 (TNFSF15), is a member of the tumor necrosis factor (TNF) family encoded by the TNFSF15 gene in humans. TL1A acts as a ligand for death receptor 3 (DR3) and decoy receptor 3 (DcR3), providing a stimulatory signal for downstream pathways. It regulates the proliferation, activation, and apoptosis of effector cells, as well as cytokine and chemokine production. TL1A is expressed in various immune cells, including monocytes, macrophages, dendritic cells, and T cells, as well as in non-immune cells such as synovial fibroblasts and endothelial cells. It plays a crucial role in modulating immune responses by promoting the differentiation and survival of T cells, particularly Th17 cells involved in inflammatory processes <sup>[6]</sup>. TL1A enhances IL-2 responses in anti-CD3/CD28-stimulated T cells and synergizes with IL-12 and IL-18 to augment IFN-γ release in human T and NK cells, biasing T cell differentiation toward a Th1 phenotype <sup>[7]</sup>. Dysregulation of TL1A expression is implicated in autoimmune diseases, including inflammatory bowel disease (IBD), rheumatoid arthritis (RA), primary biliary cholangitis (PBC), systemic lupus erythematosus (SLE), and ankylosing spondylitis (AS) <sup>[6]</sup>. TL1A has emerged as a promising therapeutic target, with ongoing research focused on developing monoclonal antibodies and other biologics to neutralize TL1A and reduce inflammation in autoimmune disorders. Clinical trial results suggest that TL1A inhibition can be used in the treatment of various autoimmune diseases, particularly IBD <sup>[8-10]</sup>.\nThe RAG2 gene encodes a protein that, together with the RAG1 protein, forms the RAG complex, playing a crucial role in V(D)J recombination during the maturation of B and T cells. During V(D)J recombination, the RAG complex attaches to the recombination signal sequences (RSS) located adjacent to V, D, or J segments in the DNA. The RAG complex cuts the DNA between the signal sequences and the segments, allowing the segments to separate and move to different regions of the genome. This process occurs repeatedly in B and T cells, arranging the V, D, and J segments in various combinations. The resulting protein diversity provides a broader capability to recognize foreign invaders, allowing the body to combat infections effectively. RAG2 is essential in V(D)J recombination, not only catalyzing the reaction but also regulating it by controlling access to specific loci. A lack of functional RAG2 protein can also lead to severe combined immunodeficie
97ncy (SCID). In mice, deleting the Rag2 gene results in the absence of V(D)J recombination, blocking the differentiation, development, and maturation of T and B cells, which lose their normal functions, leading to a SCID-like phenotype.\nThe huTL1A/huIL23A/huIL12B/Rag2-KO mouse is a model generated by crossing <a href=\"https://www.cyagen.com/mouseatlas/C001796\" style=\"color: var(--uicolor-main-color);text-decoration: underline;text-underline-offset: 4px;\" target=\"_blank\">huTL1A/huIL23A/huIL12B</a> mice (Catalog No.: <a href=\"/mouseatlas/C001796\" style=\"color: var(--uicolor-main-color);text-decoration: underline;text-underline-offset: 4px;\" target=\"_blank\">C001796</a>) with <a href=\"https://www.cyagen.com/mouseatlas/C001324\" style=\"color: var(--uicolor-main-color);text-decoration: underline;text-underline-offset: 4px;\" target=\"_blank\">Rag2-KO</a> mice (Catalog No.: <a href=\"/mouseatlas/C001324\" style=\"color: var(--uicolor-main-color);text-decoration: underline;text-underline-offset: 4px;\" target=\"_blank\">C001324</a>). This model serves as a valuable tool for studying immune-related diseases, including immune response regulation and autoimmune disorders. It provides a robust preclinical research platform for the screening, development, and safety evaluation of drugs targeting IL23A, IL12B, and TL1A.","label":"Animal Models","link":"mouseatlas/C001947","tags":[],"title":"C57BL/6Cya-<i>Tnfsf15<sup>em1(hTNFSF15)</sup>Il23a<sup>tm1(hIL23A)</sup>Il12b<sup>em1(hIL12B)</sup>Rag2<sup>em1</sup></i>/Cya"},{"description":"Programmed cell death protein 1 (PDCD1/PD-1) is a member of the B7-CD28 costimulatory receptor family. It is an inhibitory receptor expressed on activated T cells and plays a role in regulating the function of effector T cells, including CD8+ T cells, and promoting the differentiation of CD4+ T cells into regulatory T cells. PD-1 is expressed in a variety of tumors and plays an important role in antitumor immunity. In addition, PD-1 is involved in the defense against autoimmune diseases and has inhibitory effects on antitumor and antimicrobial immunity <sup>[1]</sup>.\nProgrammed cell death 1 ligand 1 (PD-L1), also known as cluster of differentiation 274 (CD274) or B7 homolog 1 (B7H1), is an immune inhibitory receptor ligand. PD-L1 is a type I transmembrane protein with immunoglobulin V-like (IgV) and C-like (IgC) structural domains and is expressed by hematopoietic and non-hematopoietic cells, including T cells, B cells, and various types of tumor cells <sup>[2]</sup>. PD-L1 can bind to the PD-1 on the surface of CD8+ T cells, inhibiting the activity of CD8+ T cells. This interaction can prevent the immune system from damaging normal tissues, but it can also be used by tumor cells to escape immune surveillance. Monoclonal antibodies that competitively bind to PD-L1 can relieve the immune function inhibition mediated by the binding of PD-1 and PD-L1. This can reactivate CD8+ T cells, triggering the human body's anti-tumor immune response <sup>[3]</sup>. Therefore, development of antibody drugs targeting PD-1 and PD-L1 is a hot area in tumor immunotherapy <sup>[3-5]</sup>.\nThe Vascular Endothelial Growth Factor (VEGF) family is a group of particular endothelial growth factors intimately associated with angiogenesis. These factors promote increased vascular permeability, extracellular matrix degeneration, vascular endothelial cell migration and proliferation, and are capable of stimulating angiogenesis and increasing the permeability of existing vessels. As such, they play a pivotal role in normal vascular development and wound healing. The VEGF family comprises VEGFA, VEGFB, VEGFC, VEGFD, VEGFE, and PLGF <sup>[6]</sup>. Of these, VEGFA is the most commonly targeted in research related to neovascular ophthalmic diseases due to its crucial role in the proliferation, migration, and formation of endothelial cell microvessels <sup>[7]</sup>. Overexpression of VEGFA in the eye can result in abnormal vascular growth and leakage, leading to various ophthalmic diseases such as Age-Related Macular Degeneration (AMD), Diabetic Retinopathy (DR), and corneal neovascularization <sup>[7-8]</sup>. The progression of solid tumors depends on vascularization and angiogenesis within malignant tissues, with VEGFA playing a crucial role among various pro-angiogenic factors. The VEGFA gene is upregulated in many known tumors, correlating with tumor staging and progression. Blocking VEGFA may lead to vascular network regression, thereby inhibiting tumor growth <sup>[9]</sup>. Thus, VEGFA is an important target for anti-angiogenic cancer therapies.\nhuPD-1/hPDL1-V/huVEGFA mouse is a triple-gene humanized model generated by crossing huPD-1/hPDL1-V mice (Catalog No.: <a href=\"/mouseatlas/I001202\" style=\"color: var(--uicolor-main-color);text-decoration: underline;text-underline-offset: 4px;\" target=\"_blank\">I001202</a>) with huVEGFA mice (Catalog No.: <a href=\"/mouseatlas/C001555\" style=\"color: var(--uicolor-main-color);text-decoration: underline;text-underline-offset: 4px;\" target=\"_blank\">C001555</a>). This model serves as a valuable tool for research on cancer immunotherapy and can also be used for the screening, development, and preclinical evaluation of PD-1/PD-L1/VEGFA-targeted drugs.","label":"Animal Models","link":"mouseatlas/C001838","tags":[],"title":"C57BL/6JCya-<i>Pdcd1<sup>em1(hPDCD1)</sup>Cd274<sup>em1(hCD274)</sup>Vegfa<sup>tm1(hVEGFA)</sup></i>/Cya"},{"description":"Programmed cell death protein 1 (PDCD1/PD-1) is a member of the B7-CD28 costimulatory receptor family. It is an inhibitory receptor expressed on activated T cells and plays a role in regulating the function of effector T cells, including CD8+ T cells, and promoting the differentiation of CD4+ T cells into regulatory T cells. PD-1 is expressed in a variety of tumors and plays an important role in antitumor immunity. In addition, PD-1 is involved in the defense against autoimmune diseases and has inhibitory effects on antitumor and antimicrobial immunity <sup>[1]</sup>. \nProgrammed cell death 1 ligand 1 (PD-L1), also known as cluster of differentiation 274 (CD274) or B7 homolog 1 (B7H1), is an immune inhibitory receptor ligand. PD-L1 is a type I transmembrane protein with immunoglobulin V-like 
97(IgV) and C-like (IgC) structural domains and is expressed by hematopoietic and non-hematopoietic cells, including T cells, B cells, and various types of tumor cells <sup>[2]</sup>. PD-L1 can bind to the PD-1 on the surface of CD8+ T cells, inhibiting the activity of CD8+ T cells. This interaction can prevent the immune system from damaging normal tissues, but it can also be used by tumor cells to escape immune surveillance. Monoclonal antibodies that competitively bind to PD-L1 can relieve the immune function inhibition mediated by the binding of PD-1 and PD-L1. This can reactivate CD8+ T cells, triggering the human body's anti-tumor immune response <sup>[3]</sup>. Therefore, developing of antibody drugs targeting PD-1 and PD-L1 is a hot area in tumor immunotherapy <sup>[3-5]</sup>.\nhuPD-1/hPDL1-V mice are PD-1 and CD274 double humanized mouse models obtained by mating PD-1 humanized mouse models with CD274 humanized mouse models. They express human PD-1 and CD274 genomic sequences under the control of mouse promoters. This model is a valuable tool for studying cancer immunotherapy. In addition, this model also provides a powerful preclinical research platform for evaluating the efficacy and mechanism of therapeutic drugs targeting PD-1 and PD-L1.","label":"Animal Models","link":"mouseatlas/I001202","tags":[],"title":"C57BL/6Cya-<i>Pdcd1<sup>em1(hPDCD1)</sup>Cd274<sup>em1(hCD274)</sup></i>/Cya"},{"description":"The IL23A gene encodes the p19 subunit, a component of interleukin-23 (IL-23), which forms a heterodimer with the p40 subunit (encoded by IL12B) to generate the functional IL-23 cytokine <sup>[1]</sup>. Primarily expressed by activated dendritic cells, macrophages, and monocytes, IL-23 signals through the IL-23 receptor (IL-23R) complex, activating the JAK-STAT pathway to promote Th17 cell differentiation and maintain IL-17 production. This process drives inflammatory responses and mucosal immunity against extracellular pathogens <sup>[1-2]</sup>. . Genetic polymorphisms within IL23A are strongly associated with autoimmune and inflammatory diseases, including psoriasis, Crohn's disease, and inflammatory bowel disease, due to dysregulated Th17 activity and chronic inflammation <sup>[1-2]</sup>. Monoclonal antibodies targeting IL-23, such as risankizumab and guselkumab, selectively block the p19 subunit, demonstrating therapeutic efficacy in psoriasis and inflammatory bowel diseases by suppressing pathogenic IL-17/Th17 pathways <sup>[3]</sup>. Also, monoclonal antibodies targeting IL-12B, such as ustekinumab, are clinically utilized for the treatment of moderate to severe psoriasis and Crohn's disease <sup>[4]</sup>. While IL-23 plays a role in protective immunity, its overactivation contributes to tissue damage in autoimmune settings, highlighting its dual function in immune regulation and disease pathogenesis <sup>[1-5]</sup>.\nTNF-like ligand 1A (TL1A), also known as TNF superfamily member 15 (TNFSF15), is a member of the tumor necrosis factor (TNF) family encoded by the TNFSF15 gene in humans. TL1A acts as a ligand for death receptor 3 (DR3) and decoy receptor 3 (DcR3), providing a stimulatory signal for downstream pathways. It regulates the proliferation, activation, and apoptosis of effector cells, as well as cytokine and chemokine production. TL1A is expressed in various immune cells, including monocytes, macrophages, dendritic cells, and T cells, as well as in non-immune cells such as synovial fibroblasts and endothelial cells. It plays a crucial role in modulating immune responses by promoting the differentiation and survival of T cells, particularly Th17 cells involved in inflammatory processes <sup>[6]</sup>. TL1A enhances IL-2 responses in anti-CD3/CD28-stimulated T cells and synergizes with IL-12 and IL-18 to augment IFN-γ release in human T and NK cells, biasing T cell differentiation toward a Th1 phenotype <sup>[7]</sup>. Dysregulation of TL1A expression is implicated in autoimmune diseases, including inflammatory bowel disease (IBD), rheumatoid arthritis (RA), primary biliary cholangitis (PBC), systemic lupus erythematosus (SLE), and ankylosing spondylitis (AS) <sup>[6]</sup>. TL1A has emerged as a promising therapeutic target, with ongoing research focused on developing monoclonal antibodies and other biologics to neutralize TL1A and reduce inflammation in autoimmune disorders. Clinical trial results suggest that TL1A inhibition can be used in the treatment of various autoimmune diseases, particularly IBD <sup>[8-10]</sup>.\nhuTL1A/huIL23A/huIL12B mouse is a triple-gene humanized model for IL23A, IL12B, and TNFSF15, generated by crossing huIL23A/huIL12B mice (Catalog No.: <a href=\"/mouseatlas/C001620\" style=\"color: var(--uicolor-main-color);text-decoration: underline;text-underline-offset: 4px;\" target=\"_blank\">C001620</a>) with huTL1A(TNFSF15) (Catalog No.: <a href=\"/mouseatlas/C001603\" style=\"color: var(--uicolor-main-color);text-decoration: underline;text-underline-offset: 4px;\" target=\"_blank\">C001603</a>). This model serves as a valuable tool for researching immune-related diseases, applicable to studies on immune response regulation and autoimmune diseases. It provides a robust preclinical research platform for the screening, development, and safety evaluation of drugs targeting IL23A/IL12B/TL1A.","label":"Animal Models","link":"mouseatlas/C001796","tags":[],"title":"C57BL/6Cya-<i>Il23a<sup>tm1(hIL23A)</sup>Il12b<sup>em1(hIL12B)</sup>Tnfsf15<sup>em1(hTNFSF15)</sup></i>/Cya"}],"meta":{"page":1,"limit":10,"total":39712}},"animal_models_query":{"page":1,"label":"Animal Models"}}}},"user":{"id":"","org":"","name":"","email":"","mobile":"","avater":"","duties":"","introduction":""}};
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