I2: Complement

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overall biological outcomes of complement activation

Back 1

lysis of cell membrane
opsonization
inflammation
solubilization and clearance of immune complexes from circulation
b-lymphocyte co-activation

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steps necessary to initiate complement activation through alternative pathway

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C3 hydrolysis/surface binding/classical lectin

Front 3

steps necessary to initiate complement activation through lectin pathway

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MBL binding to mannose

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subunits of C3 convertase in alternative pathway

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C3bBb

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subunits of C5 convertase in alternative pathway

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C3bBb3b

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C3 convertase subunits of lectin pathway

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C4b2a

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C5 convertase subunits of lectin pathway

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C4b2a3b

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MASP function

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catalyzes: C4 + C2 = C4b2a

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factor D function

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catalyzes C3bB to C3bBb

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significance of thioester bond

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creates a site that stabilizes C3b or C4b for continued complement activation

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structure of membrane attack complex of complement system

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intramembrane pore: C5b6789(9-12)

Front 12

function of membrane attack complex of complement system

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osmotic lysis

Front 13

peptides that mediate cell lysis

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C5b678(9n) or C5b678

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peptides that mediate opsonization

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C3b, C4b, (iC3b, iC4b)

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peptides that mediate solubilization/clearance of Ag-Ab

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C3b (iC3b)

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peptide mediators of chemotaxis

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C5a

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Mast cell degranulation mediators

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C5a more than C3a, C4a = anaphylatoxins

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B cell co-activation mediator

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C3d

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Complement receptors for opsonic and adhesion

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CR3, CR4 > CR1
binds C3b, C4b

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Anaphylaxis receptors

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C5aR more than C3a/4aR (mast cells, basophils, smooth muscle cells)

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complement chemotactic receptors

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C5aR (neutrophils)

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Clearance receptor for soluble immune cmoplexes

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CR1 (RBC)

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B cell co-receptor

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CR2 complex

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C4b-BP

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binds C4b and inhibits it from combining with C2a to form C3 convertase

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AI

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Anaphylatoxin inhibitor
cleaves and inactivates C3a, C4a, C5a

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Factor I

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Cleaves and inactivates C3b and C4b to iC3b and iC4b
Destroys C3 convertase activity but are still opsinons

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Factor P

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stabilizes C3 convertase

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DAF

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decay Accelerating Factor induces decay of C3 convertase on membranes

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S-protein

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prevents C5b67 from attacking near by cells and causing lysis

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Leukocyte Adhesion Defect

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recurrent bacterial infections
poor pus formation

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Leukocyte adhesion defect leads to a deficiency in

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opsonophagocytosis

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Leukocyte adhesion defect is caused by

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defective transcription of CD18 gene
can't make LFA-1, CR3, CR4 receptors

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Diagnostic laboratory tests

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Immunoassay ELIZA
Total hemolytic complement
Opsonophagocytic activity
complement fixation

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total hemolytic complement measures

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classical pathway components

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opsonophagocytic activity process

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uptake of antibody-coated bacteria by neutrophils in the presence of fresh nonimmune serum (complement)

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complement fixation tests are used in the

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diagnosis of several infectious diseases

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Paroxysmal nocturnal hemoglobinuria caused by the absence of

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DAF, CD59

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effects of paroxysmal nocturnal hemoglobinuria

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Stable membrane bound C3 convertase
sporadic hemolysis due to spontaneous C3 activation on membranes
a lot of complement activity