Invivo anti-Mouse CXCL10 (IP-10) Recombinant mAb

CXCL10, also known as interferon-gamma-inducible protein 10 (IP-10), is a small chemokine belonging to the ELR-negative CXC subfamily, with its gene also located on human chromosome 4 within the CXC chemokine gene cluster, in close proximity to CXCL9. Similar to CXCL9, CXCL10 expression is primarily driven by interferon-gamma (IFN-γ) and can be synergistically enhanced by tumor necrosis factor-alpha (TNF-α), but it can be induced in a wide variety of cell types (including monocytes, endothelial cells, fibroblasts, and tumor cells) upon infectious or inflammatory stimulation. The physiological functions of CXCL10 are highly dependent on its binding to its specific receptor CXCR3, which is highly expressed on the surface of activated T cells (particularly Th1 cells) and NK cells; thus, CXCL10 plays a central role in Th1-type immune responses by chemoattracting these immune cells to sites of infection or tumors, effectively promoting the body's anti-pathogen and anti-tumor defenses. Furthermore, like CXCL9, CXCL10 also possesses angiostatic activity due to its lack of the ELR (glutamic acid-leucine-arginine) motif, capable of inhibiting endothelial cell proliferation and neovascularization. Compared to CXCL9, CXCL10 is induced more rapidly and broadly, making it a sensitive biomarker for various inflammatory diseases, such as rheumatoid arthritis, multiple sclerosis, and viral infections (e.g., its correlation with disease severity in SARS-CoV-2 infection). In tumor immunology, CXCL10 serves both as a marker of immune activation and, in chronic inflammatory microenvironments, may promote immune exhaustion due to sustained exposure or select for tumor cell escape variants with low CXCR3 expression. Therefore, intervention strategies targeting the CXCL10-CXCR3 axis hold dual potential in both tumor immunotherapy and autoimmune disease treatment, requiring precise spatiotemporal regulation to achieve optimal efficacy.