These authors contributed equally to this study.
CD46 in innate and adaptive immunity: an update
Article first published online: 13 APR 2011
© 2011 The Authors. Clinical and Experimental Immunology © 2011 British Society for Immunology
Clinical & Experimental Immunology
Volume 164, Issue 3, pages 301–311, June 2011
How to Cite
Cardone, J., Le Friec, G. and Kemper, C. (2011), CD46 in innate and adaptive immunity: an update. Clinical & Experimental Immunology, 164: 301–311. doi: 10.1111/j.1365-2249.2011.04400.x
- Issue published online: 27 APR 2011
- Article first published online: 13 APR 2011
- Accepted for publication 4 March 2011
- autoimmune disease;
- T cell regulation
CD46 was discovered in 1986 during a search for novel C3b-binding proteins. CD46 is expressed ubiquitously and functions as a co-factor in the factor I-mediated proteolytic cleavage of C3b and C4b. Its vital role in preventing complement deposition on host tissue is underpinned by the fact that deficiency of CD46 is a predisposing factor for numerous disease conditions arising from complement-mediated ‘self-attack’. However, in the last 10 years, it has become apparent that CD46 is also heavily involved in a new and somewhat surprising functional aspect of the complement system: the down-modulation of adaptive T helper type 1 (Th1) immune responses by regulating the production of interferon (IFN)-γversus interleukin (IL)-10 within these cells. Specifically, this latter function of CD46 is a tantalizing discovery – it may not only have delivered the explanation as to why so many pathogens use and abuse CD46 as cell entry receptor but clearly has important clinical implications for the better understanding of Th1-mediated disease states and novel therapeutic approaches for their amelioration. Here, we summarize and discuss the current knowledge about CD46 and its expanding roles in the immune system.