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C4: C4 deficiency is highly associated with systemic lupus erythematosus. [3] Aβ42, a protein involved in Alzheimer's disease, can cause activation of C4 (even in plasma deficient of C1q). [18] At least one study indicates that the genetic variation of C4 plays a role in schizophrenia. [19]
Complement 4 deficiency is a genetic condition affecting complement component 4. [1] It can present with lupus-like symptoms. [2] References
Complement component 4 (C4), in humans, is a protein involved in the intricate complement system, originating from the human leukocyte antigen (HLA) system. It serves a number of critical functions in immunity, tolerance, and autoimmunity with the other numerous components.
The trimer provides a surface for interaction between the antigen-antibody complex and other complement components. The alpha chain may be cleaved to release C4 anaphylatoxin, a mediator of local inflammation. Deficiency of this protein is associated with systemic lupus erythematosus and type I diabetes mellitus.
Terminal complement pathway deficiency is a genetic condition affecting the complement membrane attack complex (MAC). It involves deficiencies of C5, C6, C7, and C8. (While C9 is part of the MAC, and deficiencies have been identified, [1] it is not required for cell lysis. [2]) People with this condition are prone to meningococcal infection. [3]
Complement component 4B (Chido blood group) is a kind of the Complement component 4 protein that in humans is encoded by the C4B gene. [ 5 ] This gene encodes the basic form of complement factor 4, part of the classical activation pathway.
Structure of mannose in its α-D mannopyranose form. Mannan is a polymer of mannose.. The lectin pathway or MBL pathway is a type of cascade reaction in the complement system, similar in structure to the classical complement pathway, [1] in that, after activation, it proceeds through the action of C4 and C2 to produce activated complement proteins further down the cascade.
Patients with LE associated with complement C4 or C2 deficiencies have a better prognosis than those without inherited deficiencies. Complement component 2 deficiency increases risk of autoimmune disorders which may be managed by receiving the adequate care.