Abstract
Complement receptor of the immunoglobulin superfamily (CRIg), also referred to as Z39Ig and V-set and Ig domain-containing 4 (VSIG4), is a single transmembrane receptor which binds complement C3b, iC3b and C3c, but not complement C3. In mice, CRIg is expressed on liver Kupffer cells and is involved in clearance of pathogens from the circulating blood. In humans, CRIg is more widely expressed on macrophages resident in various tissues including liver, lung and adipose tissue. Next to serving as a receptor for C3 molecules, CRIg extracellular domain inhibits complement activation through the alternative, but not classical, pathway. CRIg-Fc fusion proteins have been used in several preclinical in vivo studies to selectively inhibit the alternative complement pathway. Mice deficient in CRIg fail to clear pathogens efficiently and succumb to intravascular infection.
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