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Complement regulation of T cell immunity

Wing-hong Kwan1, William van der Touw, Peter S Heeger

  • 1Department of Medicine, Recanati Miller Transplant Institute and Immunology Institute, Mount Sinai School of Medicine, Box 1243, One Gustave L. Levy Plaza, New York, NY 10029, USA.

Immunologic Research
|April 6, 2012
PubMed

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.

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