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The Potential Role of Mannan‐Binding Lectin in the Clearance of Self‐Components Including Immune Complexes
Author(s) -
Saevarsdottir S.,
Vikingsdottir T.,
Valdimarsson H.
Publication year - 2004
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.0300-9475.2004.01437.x
Subject(s) - mannan binding lectin , lectin , immune system , collectin , biology , complement system , sialic acid , innate immune system , mannan , lectin pathway , c type lectin , immunology , receptor , ficolin , pattern recognition receptor , opsonin , inflammation , autoimmunity , biochemistry , classical complement pathway , phagocytosis , polysaccharide
Mannan‐binding lectin (MBL) is a pattern recognition receptor in the innate immune system. It recognizes certain sugar residues arranged in a pattern that enables MBL to bind with sufficient strength. Such sugar patterns are common on the surface of many microorganisms, and MBL has therefore been considered to be an agent that can discriminate between self and nonself. There is, however, increasing evidence supporting that MBL, like many membrane‐bound C‐type lectin‐like receptors, also helps to dispose of various outworn or abnormal body components. Most self‐components are protected with sialic acid or galactose that disrupt the pattern of the sugars that MBL can bind, but MBL may be significantly involved in the elimination of self‐components that have lost these protective terminal residues. The role of MBL in the clearance of invading pathogens has previously been thoroughly reviewed. Here, we review some findings that support the notion that MBL may contribute to noninflammatory removal of immune complexes and abnormal cells by the reticuloendothelial system. Defects in this clearance mechanism may cause an accumulation of potentially dangerous self‐components, thereby increasing the likelihood of chronic inflammation and autoimmunity.