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The classical pathway is triggered by activation of the C1-complex (C1q, C1r, and C1s), which occurs when C1q binds to IgM or IgG complexed with antigens (a single IgM can initiate the pathway, while multiple IgGs are needed), or when C1q binds directly to the surface of the pathogen. Such binding leads to conformational changes in the C1q molecule, which leads to the activation of two C1r (a serine protease) molecules. They then cleave C1s (another serine protease). The C1-complex now binds to and splits C4 and then C2, producing C4a,C4b,C2a,and C2b. The inhibition of C1r and C1s is controlled by C1-inhibitor. C4b and C2a bind to form the classical pathway C3-convertase (C4b2a complex), which promotes cleavage of C3 into C3a and C3b; C3b latter joins with C4b and C2a (the C3 convertase) to make C5 convertase (C4bC2aC3b Complex).