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![Regulation of complement system:
1- CI Inhibitor (C1-INH) Classical pathway .
2- C3a inactivator (C3a-INA; Carboxypeptidase B) It inactivates C3a.
3- Factor H & I: Alternative pathway
4- Decay accelerating factor [DAF] Both.
5- C4 binding protein (C4-BP) and Factor I Alternative .
6- Protein S (vitronectin): MAC pathway.](https://image.slidesharecdn.com/complement24new-240416214400-195169bf/75/Complement-system-proteins-and-enzymes-s-20-2048.jpg)
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Complement system proteins and enzymes s
- 1. COMPLEMENT SYSTEM Prof Dr.Naael H Ali, Ph.D Clinical Immunology Dep. of Microbiology College of Medicine University of Basrah
- 2. Introduction The term complementrefers to a set of 50-plus serum proteins that cooperates with both the innate and the adaptive immune systems to eliminate pathogens, dying cells, and immune complexes from the body . It is named “complement system” because it was first identified as a heat-labile component of serum that “complemented” antibodies in the killing of bacteria. Normally, these proteins are in an inactive form (proenzyme), but specific signal can activate the first protein
- 3. Component of Complementsystem Over 50 serum and cell surface proteins: Complement components (in serum inactive, activated sequentially as a cascade) Complement receptors (cell surface, recognize activated components) Regulatory proteins of complement (both in serum and cell surface, inhibit activated components)
- 4. Properties of Complements Source of complement proteins produced by hepatocytes, macrophages and intestinal epithelial cells. Fibroblasts and intestinal epithelial cells make C1, while the liver makes C3, C6, and C9. Heating at 56 c for 30 minutes can inactivate complements. Complete deterioration within a day or two and even in the refrigerator, considerable loss of activity occurs in 3-4 days. Complement may be destroyed by acids and alkalis, So, all glassware must be chemically clean, although not necessarily sterile. Complements may be preserved by freezing and lyophilization. Serum complement levels, especially C3, often drop during infection (complement is activated faster than it is produced).
- 5. Three pathways: 1- ClassicalPathway 2- Alternative Pathway 3- Mannose Binding-Lectine Pathway
- 7.
- 10. Major biologic activityof Complement Complement is the term applied to a plasma effector system: direct mediation of acute inflammatory reactions destruction of many kinds of cells, bacteria and viruses. Complement factors has some hormone-like properties: recruit other humoral and cellular effectors; induces directed neutrophil migration; triggers histamine release from mast cells; stimulates release of lysosomal enzymes from PMN's.
- 11. Activating Stimuli Bacterial lysisPhagocytosis Chemotaxis Vasodilation Permeability Microbial Surfaces Ag-Ab Complexes Ag-Ab Complexes Collagen base- Polysaccharides (IgG or IgM) (IgE on Mast cells) membrane (tissue injury)
- 12. Activating Stimuli Bacterial lysisPhagocytosis Chemotaxis Vasodilation Permeability Microbial Surfaces Ag-Ab Complexes Ag-Ab Complexes Collagen base- Polysaccharides (IgG or IgM) (IgE on Mast cells) membrane (tissue injury) Complement Activation Alternate Pathway C3 and C5 C3b and C5b Membrane attack complex
- 13. Activating Stimuli Bacterial lysisPhagocytosis Chemotaxis Vasodilation Permeability Microbial Surfaces Ag-Ab Complexes Ag-Ab Complexes Collagen base- Polysaccharides (IgG or IgM) (IgE on Mast cells) membrane (tissue injury) Complement Activation Alternate Pathway C3b and C5b Membrane attack complex C3 and C5 Complement Activation Classical Pathway C3b Opsonization
- 14. Activating Stimuli Bacterial lysisPhagocytosis Chemotaxis Vasodilation Permeability Microbial Surfaces Ag-Ab Complexes Ag-Ab Complexes Collagen base- Polysaccharides (IgG or IgM) (IgE on Mast cells) membrane (tissue injury) Complement Activation Alternate Pathway C3b and C5b Membrane attack complex C3 and C5 Complement Activation Classical Pathway C3b Opsonization C3a C5a (Anaphalytoxins)
- 15. Activating Stimuli Bacterial lysisPhagocytosis Chemotaxis Vasodilation Permeability Microbial Surfaces Ag-Ab Complexes Ag-Ab Complexes Collagen base- Polysaccharides (IgG or IgM) (IgE on Mast cells) membrane (tissue injury) Complement Activation Alternate Pathway C3b and C5b Membrane attack complex C3 and C5 Complement Activation Classical Pathway C3b Opsonization C3a C5a (Anaphalytoxins) Mast cell degranulation Histamine release
- 16. Activating Stimuli Bacterial lysisPhagocytosis Chemotaxis Vasodilation Permeability Microbial Surfaces Ag-Ab Complexes Ag-Ab Complexes Collagen base- Polysaccharides (IgG or IgM) (IgE on Mast cells) membrane (tissue injury) Complement Activation Alternate Pathway C3b and C5b Membrane attack complex C3 and C5 Complement Activation Classical Pathway C3b Opsonization C3a C5b (Anaphalytoxins) Mast cell degranulation Histamine release
- 17. Activating Stimuli Bacterial lysisPhagocytosis Chemotaxis Vasodilation Permeability Microbial Surfaces Ag-Ab Complexes Ag-Ab Complexes Collagen base- Polysaccharides (IgG or IgM) (IgE on Mast cells) membrane (tissue injury) Complement Activation Alternate Pathway C3b and C5b Membrane attack complex C3 and C5 Complement Activation Classical Pathway C3b Opsonization C3a C5b (Anaphalytoxins) Mast cell degranulation Histamine release Hageman factor Coagulation cascade Kallikrein Activation Bradykinin
- 18.
- 19. Diagnostic significant Increased complementactivity may be seen in: Cancer Certain infections Ulcerative colitis Decreased complement activity may be seen in: Cirrhosis Glomerulonephritis Hereditary angioedema Hepatitis Kidney transplant rejection Lupus nephritis Malnutrition Systemic lupus erythematosis
- 20. Regulation of complementsystem: 1- CI Inhibitor (C1-INH) Classical pathway . 2- C3a inactivator (C3a-INA; Carboxypeptidase B) It inactivates C3a. 3- Factor H & I: Alternative pathway 4- Decay accelerating factor [DAF] Both. 5- C4 binding protein (C4-BP) and Factor I Alternative . 6- Protein S (vitronectin): MAC pathway.