What is a stimulus for activation of complement proteins of the immune system?
Answers
Answer:
Molecular Immunology
Activation of the complement system is triggered by the presence of pathogen, altered or injured cells or other irritants and leads to the proteolytic activation of complement components C3 and C5 and generation of biologically active anaphylatoxins (C3a and C5a) and opsonins (C3b and C4b).
Explanation:
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Answer:
Immunology
Activation of the complement system is triggered by the presence of pathogen, altered or injured cells or other irritants and leads to the proteolytic activation of complement components C3 and C5 and generation of biologically active anaphylatoxins (C3a and C5a) and opsonins (C3b and C4b).
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Explanation:
The complement system plays an important role in shaping the adaptive immune response. Whereas initially the focus was mainly on B cells and antibody responses, the focus has shifted to the T cell–dendritic cell interface, and now even toward the intra-cellular environment of T cells. C3dg, a degradation product of C3b, serves as a natural adjuvant by providing co-stimulatory signals to B cells via binding to CR2 in the B cell co-receptor complex.24 In addition to activating B cells, CR2 is also involved in the capture and prolonged presentation of complement-opsonized antigens on follicular dendritic cells.15 Complement also has an impact on the effector arm of antibodies, not just via the classical pathway, but also by influencing the expression levels of cellular Fcγ receptors. C5aR triggering alters the expression levels of activating and inhibiting Fcγ receptors in such a way that cells are more prone to respond to antibody triggering.25 Interestingly, Fcγ receptor signaling can enhance synthesis of C5,26 reinforcing the C5a-Fcγ receptor cross-talk.25,26
Direct effects of complement on T cell immunity were concluded from experiments with complement-deficient animals—for example, in the context of transplant rejection.27 The local production of the anaphylatoxins C3a and C5a in the T cell–dendritic cell synapse highly determines the outcome of these cognate interactions.28 Expression levels of complement inhibitory molecules such as DAF (CD55) have an impact on the degree of complement activation and hence the degree of dendritic cell and T cell activation. In addition, specific triggering of membrane-bound complement inhibitory molecules such as CD59 and DAF can limit their activation or even skew toward a regulatory T cell phenotype.