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Vα14i NK T Cells Participate to the Early Response to MCMV Infection.
Author(s) -
Brossay Laurent,
Wesley Johnna D.,
Tessmer Marlowe S.,
Chaukos Deanna
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.856.30
Subject(s) - innate immune system , immunology , innate lymphoid cell , immune system , interleukin 21 , interleukin 12 , immunity , biology , adoptive cell transfer , natural killer t cell , t cell , virology , cytotoxic t cell , in vitro , biochemistry
Immunity to the well‐characterized virus MCMV is critically dependent on the innate response for initial control of viral replication. The contribution of innate immune cells, other than natural killer (NK) cells, to the propagation of an optimal anti‐viral immune response has not been fully examined. Therefore, we sought to determine the role and function of a unique, innate subset of T cells, Vα14 invariant natural killer T (Vα14i NK T) cells, in the anti‐viral response to MCMV infection in vivo. Vα14i NK T cells become activated and produce significant levels of IFN‐γ but not IL‐4 following MCMV infection, particularly in the liver. Adoptive transfers of Vα14i NK T cells in MCMV infected CD1d17 −/− mice demonstrate that CD1d1 is not critical for their activation. Interestingly, both IFN‐α/β and IL‐12 are partially required for their activation status. Vα14i NK T cell derived IFN‐γ is highly dependent on IL‐12 but surprisingly partially dependent of IFN‐α. Collectively, these findings highlight the unique activation requirements of these innate T cells in the induction of an anti‐viral immunity. Supported by NIH grant AI46709.