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Updated: Oct 24 2022


  • Overview
  • Introduction
    • The complement system is a group of circulating proteins that
      • are synthesized by the liver
      • participate in humoral immunity
      • act as proteases and cleave one another in cascade
      • bind to pathogens as well as immune complexes
      • alert phagocytes of the innate immune system
    • The system can be activated in one of three ways including
      • the classical pathway
        • when activated by antibodies
      • the alternative pathway
        • when activated spontaneously
      • the lectin pathway when
        • activated by mannose residues on pathogens
    • Activation of the complement pathway leads to
      • a cascading cleavage of downstream proteins
      • seperation of protein fragments after cleavage where
        • a is the smaller component that is carried by the bloodstream
        • b is the larger component that stays on the pathogen
    • Complement must be closely controlled by inhibitors such as
      • C1 esterase inhibitor
      • CD55 (decay accelerating factor)
  • Activation of Complement
      • Complement Activation Pathways
      • Feature
      • Classical
      • Alternative
      • Lectin
      • Detects
      • Surfaces with bound antibodies (IgG and IgM)
      • Surfaces not protected by complement inhibitors
      • Surfaces with mannose
      • Specificity
      • Conferred by the specific binding of antibodies
      • Conferred by inactivation of complement by host inhibitors
      • Conferred by lack of mannose on host membranes
      • Initiating factor
      • C1q 
      • C1rC1s
      • C1s
      • C3 factor turnover
      • Factor D
      • Mannose binding lectin and associated proteases
      • C3 convertase
      • C4b
      • C2b
      • C3b
      • Factor Bb
      • C4b
      • C2b
  • Functions
    • The complement cascade has many functions including
      • opsonization of invading pathogens mediated by
        • coating of pathogens by C3b and IgG
        • activation of phagocytosis by these fragments
      • clearance of immune complexes and cellular debris
      • chemotaxis of neutrophils mediated by
        • release of C5a into bloodstream after cleavage
        • detection of C5a by innate immune cells
      • direct cytolysis of pathogens through
        • formation of the membrane attack complex (MAC)
        • insertion of the MAC into bacterial membranes
        • rupture of the cell with release of internal contents
      • vascular changes such as dilation that
        • are caused by immune reaction to C3a, C4a, and C5a
          • C3a is a potent anaphylatoxin that causes mast cell degranulation, leading to vascular permeability and urticaria
        • can lead to anaphylaxis if released systemically
    • Together these effects of the complement cascade are important in
      • initial activation of the innate immune system
      • clearance of debris such as immune complexes
      • assistance with humoral immunity
  • Complement Component Deficiencies
      • Complement Component Deficiencies
      • Missing Factor
      • Presentation
      • Pathology
      • Circulating C3
      • Recurrent infection by pyogenic bacteriaIncreased susceptibility to type III hypersensitivity reactions
      • Failure of C3 convertase formation
      • Lack of immune complex and pathogenic bacterial clearance
      • C5, C6, C7, C8, or C9
      • Increased susceptibility to recurrent Neisseria infections
      • Failure of membrane attack complex formation
      • C1 esterase inhibitor
      • Hereditary angioedema
      • ACE inhibitors are contraindicated
      • Unregulated activation of kallikrein by complement system leading to increased bradykinin activity
      • Decay accelerating factor (CD55)
      • Paroxysmal nocturnal hemoglobinuria
      • Unregulated activation of complement leads to lysis of red blood cells
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