Hormonal regulation of mannan-binding lectin synthesis in hepatocytes
نویسندگان
چکیده
منابع مشابه
Introduction to mannan-binding lectin.
Mannan-binding lectin (MBL) was first discovered as a plasma opsonin for baker's yeast and was independently characterized biochemically. It belongs to the small subfamily of collectins: C-type lectins possessing a collagen-like domain. MBL is synthesized by the liver and secreted into the bloodstream. It is believed to be an important component of innate immunity, acting as an ante-antibody an...
متن کاملClinical manifestations of mannan-binding lectin deficiency.
Mannan-binding lectin (MBL) is a plasma protein of the innate immune system with the ability to initiate antimicrobial and inflammatory actions. MBL deficiency is common. More than 10% of the general population may, depending on definition, be classified as MBL deficient, underlining the redundancy of the immune system. Ongoing research attempt to illuminate at which conditions MBL deficiency m...
متن کاملMannan-Binding Lectin in Cardiovascular Disease
Cardiovascular disease remains the leading cause of mortality and morbidity worldwide so research continues into underlying mechanisms. Since innate immunity and its potent component mannan-binding lectin have been proven to play an important role in the inflammatory response during infection and ischaemia-reperfusion injury, attention has been paid to its role in the development of cardiovascu...
متن کاملMannan binding lectin deficiency and concomitant immunodefects.
OBJECTIVE To determine the prevalence of a mannan binding lectin (MBL) deficiency in children with increased susceptibility to infections and to investigate whether other coexisting immunodeficiencies affecting opsonisation are needed to render MBL deficiency clinically significant. PATIENTS AND METHODS 343 serum samples were collected from 266 children with repeated infections, a single epis...
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ژورنال
عنوان ژورنال: Clinical and Experimental Immunology
سال: 2006
ISSN: 0009-9104,1365-2249
DOI: 10.1111/j.1365-2249.2006.03101.x