Lack Of T-Cell Mediated Il2 And Tnfa Production Is Linked With The Decreased Cd58 Expression In Intestinal Tissue During Acute Simian Immunodeficiency Virus Infection
JOURNAL OF GENERAL VIROLOGY(2018)
Abstract
Abstract Human immunodeficiency virus type 1 (HIV-1)/simian immunodeficiency virus (SIV) infection causes a progressive impairment of the immune system characterized by massive CD4+ T-cell loss, CD8+ T-cell expansion and sustained immune activation and inflammation. Our data also suggest that pathogenic SIVMAC251 infection in rhesus macaques (RMs) leads to decreased production of several T-helper 1 (TH1) and TH2 cytokines and increased production of IL-17, IFNg, CCL4 and GM-CSF by intestinal CD8+ T-cells 21 days after infection. For an effective T-cell activation and response, costimulation is required in addition to the antigen-specific signal from their antigen receptors. The CD2/CD58 interaction is considered as one of the important T-cell costimulatory pathway for T-cell activation and proliferation. Intestinal lamina propria T cells were reported to be highly responsive to a stimulus delivered by CD2 pathway compared to the conventional CD3/TCR pathway. The role of CD2/CD58 in regulating intestinal T-cell function of acute and chronic SIV infected RMs is poorly documented. Here, we demonstrated a significant reduction of CD58 expression in both T- and B-cell population during acute SIV infection along with the loss of intestinal CD4+ T-cells and high plasma viral load compared to SIV-uninfected normal RMs. The reduction of CD58 expression in T-cells was positively correlated with the reduced expression of T-cell mediated IL2 and TNFa production. Together, these results indicate that the reduction in CD2/CD58 interaction pathway in mucosal lymphocytes might play a crucial role in mucosal T-cell dysfunction during acute SIV/HIV infection.
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Key words
CD2,CD58,cytokine,mucosal immunology,SIV
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