CXCL9

CXCL9, also known as MIG, is one member of the ELR-negative CXC chemokine subfamily, and can be induced by IFN-γ. CXCL9 binds to its receptor CXCR3 and can recruit CXCR3+ cells, such as effector T cells, regulatory T cells (Tregs) and CD8+ cytotoxic T cells. CXCL9 is involved in immunoregulatory and inflammatory processes, but it also play a key role in tumor growth, angiogenesis, and metastasis. CXCL9 is secreted by various cell types including immune cells (T lymphocytes, NK cells, dendritic cells, macrophages, eosinophils, etc.), and non‐immune cells (hepatic stellate cells, preadipocytes, thyrocytes, endothelial cell, tumor cells, and fibroblasts, etc)^[1].
CXCL9 is one of the ligands of chemokine receptor CXCR3 that mediates the infiltration of lymphocytes to focal sites and suppresses tumor growth. CXCL9 attracts CXCR3- (CXCR3-A and CXCR3-B) T lymphocytes, is involved in the pathogenesis of a variety of physiologic diseases during their initiation and their maintenance. The transcriptional regulation of CXCL9 is a multistep process involving many transcription factors, of which STAT1 and NF‐κB are two most well‐characterized members. Both the gene mutation of STAT1 and the blocking of the JA/STAT1 pathway can reduce CXCL9 expression induced by IFN-γ. Moreover, CXCL9 expression can be suppressed by reducing the levels of components of the STAT1-IRF‐1 transcriptional activation pathway by Porphyromonas gingivalis that leads to the immune function decline. Lipopolysaccharide (LPS) and D‐galactosamine could induce the phosphorylation of STAT1 and enhance the transcription of CXCL9 leading to the enhancement of liver inflammation, and even liver apoptosis and injury^[1][2][3].