The ITGA4 gene encodes the integrin α4 subunit, which pairs with the integrin β7 subunit, encoded by the ITGB7 gene, to form the heterodimeric transmembrane protein α4β7, a key member of the integrin protein family ^[1]. α4β7 is prominently expressed in immune tissues, including lymph nodes, bone marrow, spleen, and blood, as well as in diverse immune cell populations, such as T lymphocytes, B lymphocytes, monocytes, granulocytes, and natural killer cells ^[1]. Functionally, α4β7 mediates cell adhesion and migration, critically regulating immune cell trafficking and inflammatory processes. Specifically, α4β7 facilitates lymphocyte migration to sites of inflammation and intestinal lymphoid tissues through interactions with vascular cell adhesion molecule-1 (VCAM-1) and mucosal addressin cell adhesion molecule-1 (MAdCAM-1) ^[2]. Notably, ITGA4 and ITGB7 have been implicated in the pathogenesis of autoimmune diseases, including inflammatory bowel disease (IBD), Crohn's disease, ulcerative colitis, and multiple sclerosis ^[2-4]. Consequently, the targeting of α4β7 has emerged as a key therapeutic strategy for inflammatory and autoimmune disorders.

TNF-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 ^[5]. 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 ^[6]. 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) ^[5]. 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 ^[7-9].

B6-hα4β7/hTL1A mouse is a triple-gene humanized model for ITGA4, ITGB7, and TNFSF15, generated by crossing B6-hα4β7 mice (Catalog No.: C001689) with B6-hTL1A (TNFSF15) mice (Catalog No.: C001603). This model serves as a valuable tool for researching immune-related diseases, applicable to studies on T cell differentiation and survival, immune response regulation, and autoimmune diseases. It provides a robust preclinical research platform for the screening, development, and safety evaluation of α4β7/TL1A-targeted drugs.