Complement-dependent cytotoxicity

Complement-dependent cytotoxicity (CDC) is an effector function of IgG and IgM antibodies. When they are bound to surface antigen on target cell (e.g. bacterial or viral infected cell), the classical complement pathway is triggered by bonding protein C1q to these antibodies, resulting in formation of a membrane attack complex (MAC) and target cell lysis.

Complement system is efficiently activated by human IgG1, IgG3 and IgM antibodies, weakly by IgG2 antibodies and it is not activated by IgG4 antibodies.[1]

It is one mechanism of action by which therapeutic antibodies[2] or antibody fragments[3] can achieve an antitumor effect.[4][5]

  1. ^ Schroeder, Harry W.; Cavacini, Lisa (2010). "Structure and function of immunoglobulins". Journal of Allergy and Clinical Immunology. 2010 Primer on Allergic and Immunologic Diseases. 125 (2, Supplement 2): S41–S52. doi:10.1016/j.jaci.2009.09.046. ISSN 0091-6749. PMC 3670108. PMID 20176268.
  2. ^ The Role of Complement in the Mechanism of Action of Rituximab for B-Cell Lymphoma: Implications for Therapy. Zhou 2008
  3. ^ Complement dependent cytotoxicity activity of therapeutic antibody fragments is acquired by immunogenic glycan coupling. Archived 2016-04-09 at the Wayback Machine
  4. ^ Meyer, Saskia; Leusen, Jeanette HW; Boross, Peter (2014). "Regulation of complement and modulation of its activity in monoclonal antibody therapy of cancer". mAbs. 6 (5): 1133–1144. doi:10.4161/mabs.29670. ISSN 1942-0862. PMC 4622586. PMID 25517299.
  5. ^ Wang, Xinhua; Mathieu, Mary; Brezski, Randall J. (2018). "IgG Fc engineering to modulate antibody effector functions". Protein & Cell. 9 (1): 63–73. doi:10.1007/s13238-017-0473-8. ISSN 1674-800X. PMC 5777978. PMID 28986820.