Complement regulation of T cell immunity

Wing Hong Kwan, William Van Der Touw, Peter S. Heeger

Research output: Contribution to journalArticlepeer-review

68 Scopus citations


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.

Original languageEnglish
Pages (from-to)247-253
Number of pages7
JournalImmunologic Research
Issue number1-3
StatePublished - Dec 2012


  • Allograft rejection
  • Autoimmunity
  • Complement
  • Costimulation
  • T cells


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