Mouse Chemokine C-X-C-Motif Receptor 3 (CXCR3) Protein

Background

CXCR3 is a G protein-coupled receptor (GPCR) primarily expressed on activated T cells, natural killer (NK) cells, and some epithelial cells. It binds chemokines such as CXCL9, CXCL10, and CXCL11, which are induced by interferon-gamma during inflammation. CXCR3 plays a critical role in T cell trafficking, promoting migration to inflammatory sites and tumor microenvironments. Its activation triggers signaling pathways like PI3K, MAPK, and JAK/STAT, leading to cell migration, proliferation, and cytokine production. CXCR3 has two main isoforms, CXCR3-A and CXCR3-B, which mediate different functions: CXCR3-A drives chemotaxis and immune cell recruitment, while CXCR3-B can induce apoptosis and inhibit cell migration under specific conditions. CXCR3 is implicated in autoimmune diseases like rheumatoid arthritis, multiple sclerosis, and inflammatory bowel disease, where aberrant T cell migration leads to chronic inflammation. In cancer, CXCR3 regulates both pro- and anti-tumor responses; while it facilitates immune cell infiltration into tumors, it can also enhance tumor cell metastasis and angiogenesis in some cancers. Its expression in tumor cells has been linked to poor prognosis, particularly in melanoma, breast, and lung cancers. Pharmacological targeting of CXCR3 is being explored to modulate immune responses, reduce inflammation, and improve cancer immunotherapy. Overall, CXCR3 is essential for immune cell migration, balancing immune surveillance and disease progression.