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Biochemistry and genetics of mannan-binding lectin (MBL)
J S Presanis1, M Kojima, R B Sim
1MRC Immunochemistry Unit, Department of Biochemistry, Oxford University, South Parks Road, Oxford OX1 3QU, UK.
Biochemical Society Transactions
|July 31, 2003
Summary
Mannose-binding lectin (MBL) activates complement, aiding pathogen clearance. MBL deficiency, often due to genetic mutations, increases susceptibility to infections and inflammatory diseases.
Area of Science:
- Immunology
- Biochemistry
- Molecular Biology
Background:
- Mannose-binding lectin (MBL) is a collectin protein crucial for innate immunity.
- MBL comprises polypeptide chains with collagen-like and C-type lectin domains, forming complex structures.
- Collectins bind microbial sugar patterns, mediating effector functions like phagocytosis.
Purpose of the Study:
- To elucidate the role of MBL in complement activation and host defense.
- To investigate the structural similarities between MBL and complement protein C1q.
- To understand the impact of MBL variability and deficiency on disease susceptibility.
Main Methods:
- Structural analysis of MBL and its association with MBL-associated serine proteases (MASPs).
- Investigating the complement activation pathway initiated by MBL binding.
- Reviewing studies on human MBL serum concentration variability and its genetic basis.
Main Results:
- MBL is the sole collectin capable of activating the complement system.
- MBL activates complement via MASPs, similar to C1q, facilitating opsonization and microbial clearance.
- Genetic mutations in MBL's collagen-like region cause variability and deficiency, linked to increased infectious and inflammatory disease risk.
Conclusions:
- MBL plays a vital role in the innate immune system by activating complement.
- MBL's mechanism of complement activation is analogous to C1q.
- MBL deficiency represents a significant risk factor for various infectious and inflammatory conditions.