CTLA-4-Mediated Inhibition in Regulation of T Cell Responses: Mechanisms and Manipulation in Tumor Immunotherapy

DOI Web Site 被引用文献16件
  • Cynthia A. Chambers
    University of Massachusetts Medical School, Worcester, Massachusetts 01655
  • Michael S. Kuhns
    University of Massachusetts Medical School, Worcester, Massachusetts 01655
  • Jackson G. Egen
    University of Massachusetts Medical School, Worcester, Massachusetts 01655
  • James P. Allison
    University of Massachusetts Medical School, Worcester, Massachusetts 01655

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<jats:p>The T cell compartment of adaptive immunity provides vertebrates with the potential to survey for and respond specifically to an incredible diversity of antigens. The T cell repertoire must be carefully regulated to prevent unwanted responses to self. In the periphery, one important level of regulation is the action of costimulatory signals in concert with T cell antigen-receptor (TCR) signals to promote full T cell activation. The past few years have revealed that costimulation is quite complex, involving an integration of activating signals and inhibitory signals from CD28 and CTLA-4 molecules, respectively, with TCR signals to determine the outcome of a T cell's encounter with antigen. Newly emerging data suggest that inhibitory signals mediated by CTLA-4 not only can determine whether T cells become activated, but also can play a role in regulating the clonal representation in a polyclonal response. This review primarily focuses on the cellular and molecular mechanisms of regulation by CTLA-4 and its manipulation as a strategy for tumor immunotherapy.</jats:p>

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