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Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Immunol 2011 ; 187 (5): 2291-301 Nephropedia Template TP
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Phagocytosis, a potential mechanism for myeloid derived suppressor cell regulation of CD8+ T cell function mediated through PD-1 and PD-L1 interaction #MMPMID21795591
Kim YJ; Park SJ; Broxmeyer HE
J Immunol 2011[Sep]; 187 (5): 2291-301 PMID21795591show ga
CD8+ T cells become exhausted, inducing cell surface protein programmed cell death-1 (PD-1) as chronic virus diseases or tumors progress, but underlying mechanisms of this are unclear. We previously showed that M-CSF is important for developing tolerogenic dendritic cells (DCs) from human CD14+ monocytes. Here, we identify M-DC after stimulation with IL-10 as myeloid derived suppressor cells with additional tolerogenic activities to CD8+ T cells. IL-10 increased PD-L1 expression on M-DC, and M-DC/IL-10 cells induced expression of PD-1 on, and apoptosis of, CD8+ T cells, and phagocytosed CD8+ T cells. Enhanced phagocytic activity of M-DC/IL-10 required IFN-?, which further increased PD-L1 and PD-L2 expression on M-DC/IL-10. M-DC/IL-10/IFN-? cells were phenotypically macrophage-like cells with little or no expression of CD86, a costimulatory molecule, but with high expression levels of CD14, CD200R and CD80. No phagocytic activity was detected with GM-CSF-derived DC. We propose that phagocytosis by M-DC/IL-10/IFN-? cells, which may be DCs or alternatively a unique subset of macrophages, may be a mechanism by which IFN-? producing CD8+ T cells are tolerized following type 1 immune responses to chronic virus or tumor, and that IFN-? links effector CD8+ T cells to their phagocytic clearance.