Vγ4+ T cells regulate host immune response to West Nile virus infection

Thomas Welte, Judith Aronson, Bin Gong, Aparna Rachamallu, Nicole Mendell, Robert Tesh, Slobodan Paessler, Willi K. Born, Rebecca L. O'Brien, Tian Wang

Research output: Contribution to journalArticle

23 Scopus citations

Abstract

The Vγ4+ cells, a subpopulation of peripheral γδ T cells, are involved in West Nile virus (WNV) pathogenesis, but the underlying mechanism remains unclear. In this study, we found that WNV-infected Vγ4+ cell-depleted mice had lower viremia and a reduced inflammatory response in the brain. The Vγ4+ cells produced IL-17 during WNV infection, but blocking IL-17 signaling did not affect host susceptibility to WNV encephalitis. We also noted that there was an enhanced magnitude of protective splenic Vγ1+ cell expansion in Vγ4+ cell-depleted mice compared to that in controls during WNV infection. In addition, Vγ4+ cells of WNV-infected mice had a higher potential for producing TGF-β. The γδ T cells of WNV-infected Vγ4+ cell-depleted mice had a higher proliferation rate than those of WNV-infected controls upon ex vivo stimulation with anti-CD3, and this difference was diminished in the presence of TGF-β inhibitor. Finally, Vγ4+ cells of infected mice contributed directly and indirectly to the higher level of IL-10, which is known to play a negative role in immunity against WNV infection. In summary, Vγ4+ cells suppress Vγ1+ cell expansion via TGF-β and increase IL-10 level during WNV infection, which together may lead to higher viremia and enhanced brain inflammation.

Original languageEnglish (US)
Pages (from-to)183-192
Number of pages10
JournalFEMS Immunology and Medical Microbiology
Volume63
Issue number2
DOIs
StatePublished - Nov 1 2011

Keywords

  • Pathogenesis
  • West Nile virus
  • γδ T cell

ASJC Scopus subject areas

  • Immunology and Allergy
  • Microbiology
  • Immunology
  • Microbiology (medical)
  • Infectious Diseases

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