CXCL9 is an inflammatory chemokine initially identified by differential screening of a cDNA library from lymphokine-activated macrophages. CXCL9 is a CXC chemokine and member of the non-ELR (lacking a Glu-Leu-Arg motif in the N-terminal region) CXC chemokine family. CXCL9 shares the CXCR3 receptor with CXCL10 and CXCL11, and these ligands differ in their receptor-binding and -activating properties; CXCL11 is more potent than CXCL10, and CXCL10 is more potent than CXCL9. An alternative spliced variant, CXCR3B, has been described for CXCR3. CXCR3B mediates the angiostatic effect of CXCR3 ligands and is the receptor for PF4 (CXCL4). CXCR3B has been detected in human neoplastic tissues. CXCL9 plays a key role in leukocyte trafficking, acting on activated CD4+ Th1 cells, CD8+ T cells, IL-2 activated T lymphocytes, and NK cells. Also, CXCL9 (as well as CXCL10 and CXCL11) induces angiostatic effects in human microvacular endothelial cells. In addition, CXCL9 enhances T lymphocyte function in alloimmune response; CXCL9 induces T cells proliferation and cytokine production in an experimental model of cardiac allograft vasculopathy. CXCL9 is induced by cytokines, particularly IFNgamma during infection, injury, or immunoinflammatory responses, and it can be inactivated by CD26/dipeptidil peptidase IV after truncation by this protease. Amino-terminal truncation of CXCL9 by CD26 impairs lymphocyte chemotaxis, but the antiangiogenic activity is not affected. In rheumatoid arthritis, CXCL9 is synergistically stimulated by TNFalpha or IL-1a and IFNgamma.
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