Invivo anti-Mouse CXCL9 (MIG) Recombinant mAb

CXCL9, also known as "monokine induced by interferon-gamma" (MIG), is a small chemokine belonging to the ELR-negative CXC subfamily, with its gene located within the CXC chemokine gene cluster on human chromosome 4. Its expression is primarily driven by the Th1-type cytokine interferon-gamma (IFN-γ) and can be synergistically enhanced by tumor necrosis factor-alpha (TNF-α); additionally, type I interferons (IFN-α/β) can also induce its production under certain conditions. CXCL9 exerts its core biological functions by binding to its primary receptor CXCR3, a G protein-coupled receptor—it efficiently chemoattracts and recruits activated T lymphocytes (particularly the Th1 phenotype) and natural killer (NK) cells to sites of inflammation or tumors, serving as one of the key signaling molecules regulating T cell trafficking and tissue infiltration in vivo. Beyond its potent immune chemotactic effects, CXCL9 also exhibits significant angiostatic properties due to its lack of the ELR (glutamic acid-leucine-arginine) motif, enabling it to inhibit neovascularization—a feature that renders it important in modulating wound repair and suppressing tumor growth. Given its ability to effectively guide CD8⁺ T cells into the tumor microenvironment and enhance antitumor immune responses, CXCL9 has emerged as a target of great interest in the field of cancer immunotherapy, with combination therapeutic strategies (such as co-administration with immune checkpoint inhibitors) being actively explored.