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Complement component 3b (C3b) is a large proteolytic fragment generated from the cleavage of complement C3 during activation of the complement system. Once formed, C3b rapidly exposes a thioester bond that enables it to covalently attach to hydroxyl and amino groups on nearby cell surfaces, including pathogens and host cells. Surface-bound C3b serves as a major opsonin, enhancing phagocytosis by immune cells and promoting clearance of microbes, cell debris, and apoptotic cells[8]. On host cells, C3b acts as a critical node for regulation: binding by complement regulatory proteins such as Factor H (FH), membrane cofactor protein (MCP; CD46), or complement receptor 1 (CR1; CD35) enables inactivation and degradation of C3b, thus protecting host tissue from complement-mediated damage[2][5][6][7]. Failure of this regulation due to genetic mutations or autoantibodies can lead to uncontrolled complement activation and diseases such as atypical hemolytic uremic syndrome and age-related macular degeneration[2][4][5]. Drugs targeting C3b or its activation (e.g., eculizumab, pegcetacoplan) inhibit or modulate complement activity to treat such diseases, but long-term inhibition increases infection risk due to impaired immune surveillance. Note: - The provided target entry (“C3b and host cell surfaces”) is not the standard canonical name for a molecular target; rather, it refers to the *binding event or complex* formed when C3b covalently attaches to host cell surfaces. - The molecular target usually referred to in therapeutics and immunology is "Complement component 3b" or "C3b" (not the complex "C3b and host cell surfaces")[8]. - This means the entry is *not a precise target name* and should be flagged as **is_incorrect: true** for standard molecular target ontologies. For most structured applications, each component (“C3b” and “host cell surface”) should be considered individually or as part of a process ("C3b opsonization of host cells") rather than a unique molecular target.
Inhibition of complement activation (e.g. by blocking C3 cleavage), Blockade of opsonization, Inhibition of downstream complement effector functions
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