Immunologic Research

, Volume 54, Issue 1, pp 247–253

Complement regulation of T cell immunity

  • Wing-hong Kwan
  • William van der Touw
  • Peter S. Heeger
Immunology at Mount Sinai

DOI: 10.1007/s12026-012-8327-1

Cite this article as:
Kwan, W., van der Touw, W. & Heeger, P.S. Immunol Res (2012) 54: 247. doi:10.1007/s12026-012-8327-1

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 

Copyright information

© Springer Science+Business Media, LLC 2012

Authors and Affiliations

  • Wing-hong Kwan
    • 1
  • William van der Touw
    • 1
  • Peter S. Heeger
    • 1
  1. 1.Department of Medicine, Recanati Miller Transplant Institute and Immunology InstituteMount Sinai School of MedicineNew YorkUSA

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