The ITGB7 gene encodes the integrin β7 subunit (ITGB7), which heterodimerizes with the α4 subunit (ITGA4) to form α4β7, a transmembrane protein of the integrin 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, ITGB7 has 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.

The B6-hITGB7 mouse is a humanized model constructed using gene editing technology, where the mouse Itgb7 endogenous extracellular domain was replaced with the human ITGB7 extracellular domain. The murine signal peptide was preserved. This model can be used for studying the pathological mechanisms and therapeutic approaches of inflammatory and autoimmune diseases, and for the development of ITGB7-targeted drugs.