Immunology at Mount Sinai

Immunologic Research

, Volume 54, Issue 1, pp 247-253

Complement regulation of T cell immunity

  • Wing-hong KwanAffiliated withDepartment of Medicine, Recanati Miller Transplant Institute and Immunology Institute, Mount Sinai School of Medicine
  • , William van der TouwAffiliated withDepartment of Medicine, Recanati Miller Transplant Institute and Immunology Institute, Mount Sinai School of Medicine
  • , Peter S. HeegerAffiliated withDepartment of Medicine, Recanati Miller Transplant Institute and Immunology Institute, Mount Sinai School of Medicine Email author 

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Abstract

Results of studies published since 2002 reveal that T cells and antigen-presenting cells (APCs) produce complement proteins. The immune cell–derived, alternative pathway complement components activate spontaneously, yielding local, but not systemic, production of C3a and C5a. These anaphylatoxins bind to their respective G-protein-coupled receptors, C3aR and C5aR, expressed on both partners. The resultant complement-induced T cell activation and APC activation drive T cell differentiation, expansion and survival. Complement deficiency or blockade attenuates T cell-mediated autoimmunity and delays allograft rejection in mice. Increasing complement activation, achieved by genetic removal of the complement regulatory protein decay-accelerating factor, enhances murine T cell immunity and accelerates allograft rejection. The findings support the need for design and testing of complement inhibitors in humans.

Keywords

T cells Allograft rejection Complement Costimulation Autoimmunity