Abstract
Mannose-Binding Lectin (MBL) is a member of the collectin family and is an important protein in the immune system. It is a pathogen pattern-recognition molecule that binds to specific carbohydrate motifs on the surface of many pathogens. MBL activates complementvialectin pathway. Single nucleotide polymorphisms in the MBL gene influence serum MBL concentration and function. MBL deficiencies increase the risk of infection and disease-specific complications, especially in those who are already immune compromised with pre-existing conditions. This review discusses the molecular genetics of human MBL and the association of MBL polymorphisms with liver diseases including liver fibrosis, viral hepatitis B, viral hepatitis C, and infection post-liver transplantation.
Highlights
The complement system, a major component of innate immunity, provides immediate defence against infection and has a pro-inflammatory response
The activation of lectin pathway is similar to the classical pathway except that pathogens are directly recognised by a lectin, which includes Mannose-Binding Lectin (MBL)
MBL acts as a recognition molecule for Pathogen-Associated Molecular Patterns (PAMPS) which play a role in the initiation and regulation of the immune response [11]
Summary
The complement system, a major component of innate immunity, provides immediate defence against infection and has a pro-inflammatory response It consists of plasma and membrane proteins, which mediate 3 pathways, namely classical, alternative and the most recently described lectin [1]. Activation of these pathways of cascading enzymatic reactions results in the deposition of fragments that promote inflammatory and immune response. CRD is able to form bonds with hydroxyl groups on specific ligands, including mannan, N-acetylglucosamine and glucose [10] These carbohydrates are found on pathologic microorganisms, such as bacteria, fungi, parasitic protozoans and viruses. MBL protein is, able to distinguish self from non-self in initiating the innate immune pathway
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