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Background  T cell specific adapter protein (TSAd), encoded by the  SH2D2A  gene, modulates signaling downstream of the T cell receptor (TCR). Young, unchallenged  SH2D2A -deficient C57BL/6 mice exhibit a relatively normal immune phenotype. To address whether  SH2D2A  regulates physiologic immune responses,  SH2D2A -deficient TCR-transgenic BALB/c mice were generated. The transgenic TCR recognizes a myeloma-derived idiotypic (Id) peptide in the context of the major histocompatibility complex (MHC) class II molecule I-E d , and confers T cell mediated resistance to transplanted multiple myeloma development  in vivo .    Principal Findings  The immune phenotype of  SH2D2A -deficient C57BL/6 and BALB/c mice did not reveal major differences compared to the corresponding wild type mice. When challenged with myeloma cells, Id-specific TCR-transgenic BALB/c mice lacking  SH2D2A  displayed increased resistance towards tumor development. Tumor free TCR-transgenic  SH2D2A -deficient mice had higher numbers of Id-specific single positive CD4+ thymocytes compared to TCR-transgenic wild-type mice.    Conclusion  Our results suggest a modulatory role for  SH2D2A  in T cell mediated immune surveillance of cancer. However, it remains to be established whether its effect is T-cell intrinsic. Further studies are required to determine whether targeting  SH2D2A  function in T cells may be a potential adjuvant in cancer immunotherapy.

SH2D2A Modulates T Cell Mediated Protection to a B Cell Derived Tumor in Transgenic Mice