MBL: the complement PRR
Mannose-binding lectin, also called mannose-binding protein or mannan-binding protein (MBP), is a C-type lectin that plays an important role in the innate response. MBL belongs to the collectin family of proteins that consists of a collagen-like domain and a carbohydrate recognition domain. As a pattern recognition receptor, MBL recognizes carbohydrates found on the surface of pathogens such as bacteria, viruses, fungi and protozoa. Binding of MBL to such a micro-organism results in the activation of the lectin pathway and ultimately to C3 convertase. The lectin pathway is antibody and C1q-independent and is, therefore, independent of the classical and alternative complement activation pathway.
MBL was first described in scientific papers in the early nineties. Since then it has been a topic of discussion in hundreds of scientific papers. Due to its regulatory and signaling function a multitude of conditions are associated with impaired levels of MBL:
– MBL is associated with infection and disease progression in HIV.
– Activation of MBL alters the risk or progression of multiple sclerosis.
– MBL insufficiency may be a contributing pathogenic factor in rheumatoid arthritis.
– Heart transplant recipients with MBL deficiency had fewer acute graft rejection episodes.
– MBL deficiency is associated with thrombotic events in heart disease.
– MBL depositions are found in the glomeruli of patients with glomerulonephritis.
– Sterile inflammation in the brain leading to psychotic disorders may be initiated by the MBL–MASP pathway.
– MBL seems to play a role in the immunopathogenesis of type 1 diabetes.
– MBL increases in brain injury and is associated with injury severity.
Interesting to note is that one of the common topics of discussion are the polymorphisms of MBL that cause an inherited defect in opsonization. As a pattern recognition receptor, MBL demonstrates to be one of the broadest complement markers that are pivotal in evaluating the innate immune response.
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