The quantification of human complement C7, pivotal in the terminal complement complex (TCC) or membrane attack complex (MAC), is facilitated by HK3029. C7 is integral to the MAC’s assembly, which is triggered by C5b after C5 cleavage and culminates in the polymerization of C9 and final formation of C5b9 complex, leading to cell lysis. Notably, C7 transitions from a hydrophilic to amphiphilic state post-activation, a critical step for MAC’s membrane attachment. Given its source in polymorphonuclear leukocytes and its secretion during inflammation, C7’s polymorphism, particularly the C7 M allotype identified by monoclonal antibody WU 4-15, is significant. This allotype’s prevalence in populations suggests a role in localized immune responses, adding a layer of complexity to C7’s involvement in immune regulation. Complement C7 has been associated with the pathogenesis of neurodegenerative conditions, including Alzheimer’s disease and amyotrophic lateral sclerosis (ALS). Studies have pinpointed a missense mutation in the C7 gene—rs3792646 (p.K420Q)—that is linked with an accelerated onset and exacerbated progression of Alzheimer’s. This particular mutation is also associated with reduced hippocampal volume and compromised working memory, suggesting it may influence the disease’s onset. Additionally, altered forms of C7 are noted to interfere with neuronal viability and the immune response, thereby affecting amyloid beta processing and synaptic function. It is also suggested that complement dysregulation and low C7 levels are associated with active Long Covid.
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