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How does MCP (membrane cofactor protein) stop the complement pathway on human cells?

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Final answer:

MCP (membrane cofactor protein) protects human cells by serving as a cofactor for factor I, which degrades the key complement component C3b, preventing the formation of C3 convertase and subsequent activation of the complement pathway that could lead to cell lysis.

Step-by-step explanation:

Membrane cofactor protein (MCP) plays a vital role in protecting human cells from being attacked by their own complement system, a part of the immune system that helps clear pathogens. When the complement system is activated, complement proteins bind to the surface of a pathogen.

In the alternative pathway, C3 convertase spontaneously cleaves C3 into C3b, which opsonizes pathogens, and C3a, which attracts phagocytes. The classical pathway is antibody-dependent and is initiated when C1 binds to an antigen-antibody complex, leading to the sequential activation of the complement pathway.

Subsequently, a membrane attack complex (MAC) may form, creating pores in microbial cell membranes and possibly leading to cell lysis.

MCP hinders the complement pathway by serving as a cofactor for the enzyme factor I, which degrades C3b into inactive fragments, thus preventing the formation of C3 convertase and ultimately stopping the progression of the complement cascade on human cells.

This regulation is crucial for discriminating between pathogens and host cells, ensuring that host cells remain unharmed by the complement's potent destructive capability.

Endogenous regulatory proteins like MCP prevent the complement complex from binding to human cells, differentiating them from pathogens which lack such protective proteins.

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