Premium
Regulation of Acquired Immunity by γδ T‐Cell/Dendritic‐Cell Interactions
Author(s) -
SHRESTHA NIRAJ,
IDA JAMES A.,
LUBINSKI A. STEVEN,
PALLIN MARIA,
KAPLAN GILLA,
HASLETT PATRICK A.J.
Publication year - 2005
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1358.011
Subject(s) - t cell , biology , priming (agriculture) , immune system , antigen presenting cell , immunology , dendritic cell , microbiology and biotechnology , botany , germination
A bstract : In humans, innate immune recognition of mycobacteria, including Mycobacterium tuberculosis and Mycobacterium leprae , involves toll‐like receptor‐2 (TLR‐2), expressed on immature dendritic cells (DCs), and the T‐cell γδ receptor expressed by a subpopulation of T cells that utilize Vδ2 (Vδ2 T cells). To investigate modulatory relationships between these host‐cell populations in a microbial context, in vitro experiments were performed with human DCs and Vδ2 T cells stimulated with model TLR‐2 ligands and phosphoantigens, respectively. We observed that TLR‐2‐stimulated DCs enhanced interferon‐γ (IFN‐γ) production by Vδ2 T cells; conversely, activated Vδ2 T cells enhanced TLR‐2‐induced DC maturation via soluble factors including IFN‐γ, which costimulated interleukin‐12 (IL‐12) p70 secretion by DCs. Exposure of DCs to activated Vδ2 T cells was critical for Th1 T‐cell priming when TLR‐2 stimulation was limiting. These results suggest that Vδ2 T cells may play an adjuvant role in priming protective antimycobacterial immunity when TLR‐2 stimulation is lacking, as may occur if the infectious inoculum is small, or if the pathogen is an intrinsically weak activator of DCs.