Engagement of NKp30 on Vδ1 T cells induces the production of CCL3, CCL4, and CCL5 and suppresses HIV-1 replication

Kelly Hudspeth, Manuela Fogli, Daniel V. Correia, Joanna Mikulak, Alessandra Roberto, Silvia Della Bella, Bruno Silva-Santos, Domenico Mavilio

Research output: Contribution to journalArticle

Abstract

Natural cytotoxicity receptors (NCRs) were originally identified as specific natural killer cell activating receptors that, on binding to their endogenous ligands, trigger the killing of tumor cell targets. We recently described the differentiation of a novel subset of NCR + V81 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 VS1 T cells after 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 CD4 +/CCR5 + infected PM1 cell lines. This experimental evidence disclosing an unanticipated antiviral function of NCR + VS1 T cells opens new avenues for understanding the pathogenic role and for manipulating the function of γδ T cells in HIV-1 infection.

Original languageEnglish
Pages (from-to)4013-4016
Number of pages4
JournalBlood
Volume119
Issue number17
DOIs
Publication statusPublished - Apr 19 2012

ASJC Scopus subject areas

  • Hematology
  • Biochemistry
  • Cell Biology
  • Immunology

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