Mannan-binding lectin pathway
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The Mannan-binding lectin pathway is homologous to the classical complement pathway. This pathway uses a protein similar to C1q of the classical complement pathway, which binds to mannose residues and other sugars in a pattern that allows binding on multiple pathogens. Mannan-binding lectin (MBL; also called mannose-binding lectin) is a protein belonging to the collectin family that is produced by the liver and can initiate the complement cascade by binding to pathogen surfaces.
MBL is a 2-6 headed molecule that forms a complex with MASP-I (Mannan-binding lectin Associated Serine Protease) and MASP-II, two protease zymogens. MASP-I and MASP-II are very similar to C1r and C1s molecules of the classical complement pathway and are thought to have a common evolutionary ancestor. When the carbohydrate-recognising heads of MBL bind to specifically arranged mannose residues on the phospholipid bilayer of a pathogen, MASP-I and MASP-II are activated to cleave complement components C4 and C2 into C4a, C4b, C2a, and C2b. C4b and C2b combine on the surface of the pathogen to form C3 convertase (C4b2b), while C4a and C2a act as chemoattractants.
Clinical significance
It has been found that people deficient in MBL experience a substantial increase in infections during the early years of childhood.
See also
External links
Immune system / Immunology | |
|---|---|
| Systems | Adaptive immune system vs. Innate immune system • Humoral immune system vs. Cellular immune system • Complement system (Anaphylatoxins) • Intrinsic immune system |
| Antibodies and antigens | Antibody (Monoclonal antibodies, Polyclonal antibodies, Autoantibody) • Allotype • Isotype • Idiotype • Antigen (Superantigen) |
| Immune cells | White blood cells (T cell, B cell, NK cell, Mast cell, Basophil, Eosinophil) • Phagocyte (Neutrophil, Macrophage, Dendritic cell) • Antigen-presenting cell • Reticuloendothelial system |
| Immunity vs. tolerance | Immunity • Autoimmunity • Allergy • Tolerance (Central) • Immunodeficiency |
| Immunogenetics | Somatic hypermutation • V(D)J recombination • Immunoglobulin class switching • MHC / HLA |
| Substances | Cytokines • Opsonin • Cytolysin |
| Other | Inflammation • Epitope (Hapten) • Cross-reactivity |
Proteins: complement system (C, L, A) | |
|---|---|
| Activators | CLA: C3-convertase - MAC (C6, C7, C8, C9) - L: Mannan-binding lectin - A: Factor P/Properdin |
| Enzymes | C: C1Q/C1R/C1S - C4 - C2 - CLA: C3 - C5 (C5a) - L: MASP1 - MASP2 - A: Factor B - Factor D |
| Inhibitors | CLA: C1-inhibitor - Decay accelerating factor - Factor I - CL: C4BP - A: Factor H |
| Complement receptors | CR1 - CR2 - CR3 - CR4 - CD11b/CD11c/CD18 - Anaphylatoxin (C3a, C5a) |
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
