Myeloid derived suppressor cells potentiate virus-specific memory CD8+ T cell response
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Updated: Jul 8, 2025

Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice
Published on: June 22, 2016
Roman Sarkar1, Mohammad Shaaz1, Sharvan Sehrawat1
1Department of Biological Sciences, Indian Institute of Science Education and Research Mohali, Sector 81, SAS Nagar Knowledge City PO Manauli, Mohali 140306, Punjab, India.
How therapeutically administered myeloid derived suppressor cells (MDSCs) modulate differentiation of virus-specific CD8+ T cell was investigated. In vitro generated MDSCs from bone marrow precursors inhibited the expansion of stimulated CD8+ T cells but the effector cells in the recipients of MDSCs showed preferential memory transition during Influenza A virus (IAV) or an α- (Herpes Simplex Virus) as well as a γ- (murine herpesvirus 68) herpesvirus infection. Memory CD8+ T cells thus generated constituted a heterogenous population with a large fraction showing effector memory (CD62LloCCR7-) phenotype. Such cells could be efficiently recalled in the rechallenged animals and controlled the secondary infection better. Memory potentiating effects of MDSCs occurred irrespective of the clonality of the responding CD8+ T cells as well as the nature of infecting viruses. Compared to the MDSCs recipients, effector cells of MDSCs recipients showed higher expression of molecules known to drive cellular survival (IL-7R, Bcl2) and memory formation (Tcf7, Id3, eomesodermin). Therapeutically administered MDSCs not only mitigated the tissue damaging response during a resolving IAV infection but also promoted the differentiation of functional memory CD8+ T cells. Therefore, MDSCs therapy could be useful in managing virus-induced immunopathological reactions without compromising immunological memory.
How therapeutically administered myeloid derived suppressor cells (MDSCs) modulate differentiation of virus-specific CD8+ T cell was investigated. In vitro generated MDSCs from bone marrow precursors inhibited the expansion of stimulated CD8+ T cells but the effector cells in the recipients of MDSCs showed preferential memory transition during Influenza A virus (IAV) or an α- (Herpes Simplex Virus) as well as a γ- (murine herpesvirus 68) herpesvirus infection. Memory CD8+ T cells thus generated constituted a heterogenous population with a large fraction showing effector memory (CD62LloCCR7-) phenotype. Such cells could be efficiently recalled in the rechallenged animals and controlled the secondary infection better. Memory potentiating effects of MDSCs occurred irrespective of the clonality of the responding CD8+ T cells as well as the nature of infecting viruses. Compared to the MDSCs recipients, effector cells of MDSCs recipients showed higher expression of molecules known to drive cellular survival (IL-7R, Bcl2) and memory formation (Tcf7, Id3, eomesodermin). Therapeutically administered MDSCs not only mitigated the tissue damaging response during a resolving IAV infection but also promoted the differentiation of functional memory CD8+ T cells. Therefore, MDSCs therapy could be useful in managing virus-induced immunopathological reactions without compromising immunological memory.
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