Journal
MOLECULAR IMMUNOLOGY
Volume 46, Issue 14, Pages 2753-2766Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.molimm.2009.04.027
Keywords
Complement; Anaphylatoxins; Inflammation; Sepsis; Allergy; Alzheimer disease; Adaptive immunity
Categories
Funding
- NIAID NIH HHS [AI057839, R01 AI059305-05, AI059305, R01 AI057839-05, R01 AI059305, R01 AI057839, R21 AI059305] Funding Source: Medline
- NIA NIH HHS [P01 AG000538, P50 - AG 00538] Funding Source: Medline
- NINDS NIH HHS [NS-35144, NS-007444, R01 NS035144, T32 NS007444] Funding Source: Medline
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The anaphylatoxin (AT) C3a, C5a and C5a-desArg are generally considered pro-inflammatory polypeptides generated after proteolytic cleavage of C3 and C5 in response to complement activation. Their well-appreciated effector functions include chemotaxis and activation of granulocytes, mast cells and macrophages. Recent evidence suggests that ATs are also generated locally within tissues by pathogen-, cell-, or contact system-derived proteases. This local generation of ATs is important for their pleiotropic biologic effects beyond inflammation. The ATs exert most of the biologic activities through ligation of three cognate receptors, i.e. the C3a receptor, the C5a receptor and the C5a receptor-like, C5L2. Here, we will discuss recent findings suggesting that ATs regulate cell apoptosis, lipid metabolism as well as innate and adaptive immune responses through their impact on antigen-presenting cells and T cells. As we will outline, such regulatory functions of ATs and their receptors play important roles in the pathogenesis of allergy, autoimmunity, neurodegenerative diseases, cancer and infections with intracellular pathogens. (C) 2009 Elsevier Ltd. All rights reserved.
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