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Activation of T Cells by Cross‐Linking Qa‐2, the Ped Gene Product, Requires Fyn
Author(s) -
De Fazio Sally R.,
Warner Carol M.
Publication year - 2007
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/j.1600-0897.2007.00503.x
Subject(s) - fyn , microbiology and biotechnology , t cell , proto oncogene tyrosine protein kinase src , protein kinase b , cell growth , src family kinase , kinase , biology , cd28 , signal transduction , cancer research , chemistry , immunology , biochemistry , immune system
Problem Qa‐2, the product of the Ped (preimplantation development) gene, regulates the rate of cell division of preimplantation mouse embryos by an unknown mechanism. Due to the limited availability of preimplantation embryos, T cells were used as a model system to assess the possible roles of Fyn and Lck, and two downstream effectors, PI‐3 kinase and Akt, in Qa‐2 induced cell proliferation. Method of study Resting T cells were stimulated to proliferate by treating with mouse anti‐Qa‐2 antibody, cross‐linking with anti‐mouse immunoglobulin, and adding PMA. The effects of kinase inhibitors on this proliferation were studied. Co‐immunoprecipitates of T‐cell lysates were analyzed for possible associations between Qa‐2 and Fyn or Lck. Fyn knockout mice (Fyn−/−) were used to determine whether Fyn is required for T‐cell activation induced by cross‐linking Qa‐2. Results An inhibitor of Src family kinases and inhibitors of PI‐3 kinase and Akt suppressed proliferation of resting T cells induced by cross‐linking Qa‐2. Fyn, but not Lck, co‐immunoprecipitated with Qa‐2. Fyn−/− T cells failed to proliferate in response to Qa‐2 cross‐linking. Conclusion Fyn, PI‐3 kinase, and Akt are required for the activation of T cells by cross‐linking Qa‐2.