Activation of VIP signaling enhances immunosuppressive effect of MDSCs on CMV-induced adaptive immunity

被引:8
作者
Forghani, Parvin [1 ]
Petersen, Christopher T. [1 ]
Waller, Edmund K. [1 ]
机构
[1] Emory Univ, Dept Hematol & Med Oncol, Winship Canc Inst, Atlanta, GA 30322 USA
关键词
CMV; myeloid-derived suppressor cells (MDSC); VIP; mice; Immunology and Microbiology Section; Immune response; Immunity; VASOACTIVE-INTESTINAL-PEPTIDE; SUPPRESSOR-CELLS; TUMOR MICROENVIRONMENT; TROPHOBLAST CELLS; BREAST-CANCER; IMMUNOMODULATION; TOLERANCE; MODEL; MICE;
D O I
10.18632/oncotarget.20704
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Vasoactive intestinal peptide (VIP) is recognized as a potent anti-inflammatory factor which affects both the innate and adaptive arms of the immune system. These effects include, but are not limited to, inhibition of T cell proliferation and disruption of immune homeostasis. Myeloid-derived suppressor cells (MDSC) are an immune regulatory cell type that has been described in settings of cancer and infectious disease. Here we demonstrate a reduced circulating monocytic MDSCs in the VIP-/- vs. wild type MCMV. VIP-/-MDSCs secretes less NO upon stimulation with LPS and interferon that relatively lose the ability to suppress T cells activation in vitro compared to wild type MDSCs. Considering the importance of VIP in immunomodulation, the possible effect of VIP in the suppressive function of MDSC populations following CMV infection remains unknown. We describe the possible role of VIP in the regulation of anti-CMV activity of T cells through the activation of MDSCs.
引用
收藏
页码:81873 / 81879
页数:7
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