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

Parvin Forghani; Christopher T. Petersen; Edmund K. Waller

doi:10.18632/oncotarget.20704

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Research Papers: Immunology:

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

Parvin Forghani, Christopher T. Petersen and Edmund K. Waller _

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Oncotarget. 2017; 8:81873-81879. https://doi.org/10.18632/oncotarget.20704

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Abstract

Parvin Forghani1,*, Christopher T. Petersen1,* and Edmund K. Waller1

1 Department of Hematology and Medical Oncology, Winship Cancer Institute, Emory University, Atlanta, Georgia, USA

* These authors have contributed equally to this work

Correspondence to:

Parvin Forghani, email:

Edmund K. Waller, email:

Keywords: CMV, myeloid-derived suppressor cells (MDSC), VIP, mice, Immunology and Microbiology Section, Immune response, Immunity

Received: June 01, 2017 Accepted: August 14, 2017 Published: September 07, 2017

Abstract

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.

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Research Papers: Immunology:

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

Abstract