Open AccessV γ4 + T cells regulate host immune response to W est N ile virus infection
Author(s) -
Welte Thomas,
Aronson Judith,
Gong Bin,
Rachamallu Aparna,
Mendell Nicole,
Tesh Robert,
Paessler Slobodan,
Born Willi K.,
O'Brien Rebecca L.,
Wang Tian
Publication year - 2011
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2011.00840.x
Subject(s) - viremia , biology , immune system , virology , viral encephalitis , immunology , t cell , inflammation , encephalitis , pathogenesis , virus
The V γ4 + cells, a subpopulation of peripheral γδ T cells, are involved in W est N ile virus ( WNV ) pathogenesis, but the underlying mechanism remains unclear. In this study, we found that WNV ‐infected V γ4 + cell‐depleted mice had lower viremia and a reduced inflammatory response in the brain. The V γ4 + 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 V γ1 + cell expansion in V γ4 + cell‐depleted mice compared to that in controls during WNV infection. In addition, V γ4 + cells of WNV ‐infected mice had a higher potential for producing TGF ‐β. The γδ T cells of WNV ‐infected V γ4 + cell‐depleted mice had a higher proliferation rate than those of WNV ‐infected controls upon ex vivo stimulation with anti‐ CD 3, and this difference was diminished in the presence of TGF ‐β inhibitor. Finally, V γ4 + 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, V γ4 + cells suppress V γ1 + cell expansion via TGF ‐β and increase IL ‐10 level during WNV infection, which together may lead to higher viremia and enhanced brain inflammation.