Abstract
Complement is an innate immune system that is a first line of defense against pathogens and facilitates elimination of apoptotic and injured cells. During complement activation, the complement convertases are assembled on target surfaces and initiate their proteolytic activities, a process that marks targets for phagocytosis and/or lysis. The complement alternative activation pathway has been implicated in a number of autoimmune conditions including arthritis and age-related macular degeneration. Properdin, a plasma component that is also released by activated neutrophils, is critical in the stabilization of alternative pathway convertases. Recently, it has been shown that properdin is also a pattern-recognition molecule that binds to certain microbial surfaces, apoptotic cells, and necrotic cells. Once bound to a surface, properdin can direct convertase formation and target uptake. New studies are now focusing on a role for properdin in inflammatory and autoimmune diseases. This review examines the new properdin findings and their implications.
Original language | English |
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Journal | Annual Review of Immunology |
Volume | 28 |
Pages (from-to) | 131-155 |
Number of pages | 25 |
ISSN | 0732-0582 |
DOIs | |
Publication status | Published - 23.04.2010 |
Research Areas and Centers
- Academic Focus: Center for Infection and Inflammation Research (ZIEL)