loop also promotes CXCL9 release. Immune cells, like Th1, CTLs, NK cells, and NKT cells, show anti-tumor effect against cancer cells through paracrine CXCL9/CXCR3 in tumor models. The autocrine CXCL9/CXCR3 signaling in cancer cells increases cancer cell proliferation, angiogenesis, and metastasis. CXCL9/CXCR3 and the PDL-1/PD-1 The relationship between CXCL9/CXCR3 and the PDL-1/PD-1 is an important area of research. Programmed cell death-1 (PD-1) is heavily expressed on T cells at the tumor site than on T cells present in the peripheral blood and anti-PD-1 therapy can inhibit “immune escape” and the immune activation. Peng et al. showed that anti-PD-1 could not only enhance T cell-mediated tumor regression but also increase the expression of IFN-γ but not CXCL9 by bone marrow–derived cells. Blockade of the PDL-1/PD-1 axis in T cells may trigger a positive feedback loop at the tumor site through the CXCL9/CXCR3 axis. Also using anti-CTLA4 antibody, this axis was significantly up-regulated in pretreatment melanoma lesions in patients with good clinical response after ipilimumab administration. CXCL9 and melanoma CXCL9 has also been identified as candidate biomarker of adoptive T cell transfer therapy in metastatic melanoma. The role of CXCL9/CXCR3 in TME and immune response - this plays a critical role in immune activation through paracrine signaling, impacting efficacy of cancer treatments. References Further reading External links Cytokines