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Abstract

Natural Cytotoxicity Receptors (NCRs) were originally identified as specific natural killer cell activating receptors that, upon binding to their endogenous ligands, trigger the killing of tumor cell targets. We recently described the differentiation of a novel subset of NCRpos Vδ1 T-cells characterized by a remarkably high cytolytic potential against cancer cells. Here, we demonstrate that the engagement of NKp30, one of the NCRs expressed de novo on Vδ1 T-cells following stimulation, triggers the production of high levels of CCL3/MIP-1α, CCL4/ MIP-1β and CCL5/RANTES but not of CXCL12/SDF-1. In turn, this NKp30-induced secretion of cc-chemokines is able to significantly suppress the replication of a CCR5 tropic strain of HIV-1 in CD4pos/CCR5pos infected PM1 cell lines. This experimental evidence disclosing an unanticipated antiviral function of NCRpos Vδ1 T-cells opens new avenues for understanding the pathogenic role and for manipulating the function of γδ T-cells in HIV-1 infection.

  • Submitted November 4, 2011.
  • Accepted February 28, 2012.