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Complement in autoimmunity and tissue injury

Complement in autoimmunity and tissue injury Autoimmunity, August 2006; 39(5): 355–356 INTRODUCTION Complement in autoimmunity and tissue injury GEORGE C. TSOKOS1 & FRANCESCO TEDESCO2,* 1 Walter Reed Army Institute of Research, Silver Spring, MD 20910, USA, and 2Department of Physiology and Pathology, University of Trieste, Trieste, Italy It is now clear that complement has two sides when it relates to autoimmunity. It has been well established that lack of early factors of complement facilitate or even instigate the development of systemic autoimmunity and specifically, systemic lupus erythematosus (SLE). It has also been well established that activation of complement contributes effectively to tissue pathology and its inhibition could herald significant clinical benefit. In this issue we have invited distinguished colleagues to contribute chapters covering both faces of this Janus-like system of proteins. In the first manuscript Erdei and her colleagues discuss the role of complement receptor 2 in the regulation of the B cell response and how its presence or absence regulates the expression of autoimmunity in animal models. Lewis and Botto present mechanisms whereby deficiencies of early complement components leads to the expression of autoimmunity. Specifically, the authors entertain the hypotheses that have been formulated to explain how C1q deficiency in men and mice http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Autoimmunity Informa Healthcare

Complement in autoimmunity and tissue injury

Abstract

Autoimmunity, August 2006; 39(5): 355–356 INTRODUCTION Complement in autoimmunity and tissue injury GEORGE C. TSOKOS1 & FRANCESCO TEDESCO2,* 1 Walter Reed Army Institute of Research, Silver Spring, MD 20910, USA, and 2Department of Physiology and Pathology, University of Trieste, Trieste, Italy It is now clear that complement has two sides when it relates to autoimmunity. It has been well established that lack of early factors of complement facilitate or even instigate the development of systemic autoimmunity and specifically, systemic lupus erythematosus (SLE). It has also been well established that activation of complement contributes effectively to tissue pathology and its inhibition could herald significant clinical benefit. In this issue we have invited distinguished colleagues to contribute chapters covering both faces of this Janus-like system of proteins. In the first manuscript Erdei and her colleagues discuss the role of complement receptor 2 in the regulation of the B cell response and how its presence or absence regulates the expression of autoimmunity in animal models. Lewis and Botto present mechanisms whereby deficiencies of early complement components leads to the expression of autoimmunity. Specifically, the authors entertain the hypotheses that have been formulated to explain how C1q deficiency in men and mice
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