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StatPearls [Internet].

Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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Madame Curie Bioscience Database [Internet].

Austin (TX): Landes Bioscience; 2000-2013.

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Immunobiology: The Immune System in Health and Disease. 5th edition.

Janeway CA Jr, Travers P, Walport M, et al.

New York: Garland Science; 2001.

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Autoimmunity: From Bench to Bedside [Internet].

Anaya JM, Shoenfeld Y, Rojas-Villarraga A, et al., editors.

Bogota (Colombia): El Rosario University Press; 2013 Jul 18.

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Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis.

Arvin A, Campadelli-Fiume G, Mocarski E, et al., editors.

Cambridge: Cambridge University Press; 2007.

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Endotext [Internet].

Feingold KR, Anawalt B, Blackman MR, et al., editors.

South Dartmouth (MA): MDText.com, Inc.; 2000-.

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Medical Microbiology. 4th edition.

Baron S, editor.

Galveston (TX): University of Texas Medical Branch at Galveston; 1996.

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Catalyzing Inquiry at the Interface of Computing and Biology.

National Research Council (US) Committee on Frontiers at the Interface of Computing and Biology; Wooley JC, Lin HS, editors.

Washington (DC): National Academies Press (US); 2005.

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Streptococcus pyogenes: Basic Biology to Clinical Manifestations [Internet]. 2nd edition.

Ferretti JJ, Stevens DL, Fischetti VA, editors.

Oklahoma City (OK): University of Oklahoma Health Sciences Center; 2022 Oct 8.

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Streptococcus pyogenes : Basic Biology to Clinical Manifestations [Internet].

Ferretti JJ, Stevens DL, Fischetti VA, editors.

Oklahoma City (OK): University of Oklahoma Health Sciences Center; 2016-.

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Polymicrobial Diseases.

Brogden KA, Guthmiller JM, editors.

Washington (DC): ASM Press; 2002.

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Immunodeficient Rodents: A Guide to Their Immunobiology, Husbandry, and Use.

National Research Council (US) Committee on Immunologically Compromised Rodents.

Washington (DC): National Academies Press (US); 1989.

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Adverse Effects of Vaccines: Evidence and Causality.

Committee to Review Adverse Effects of Vaccines; Institute of Medicine; Stratton K, Ford A, Rusch E, et al., editors.

Washington (DC): National Academies Press (US); 2011 Aug 25.

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PDQ Cancer Information Summaries [Internet].

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Molecular Biology of the Cell. 4th edition.

Alberts B, Johnson A, Lewis J, et al.

New York: Garland Science; 2002.

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Biologic Markers in Pulmonary Toxicology.

National Research Council (US) Committee on Biologic Markers.

Washington (DC): National Academies Press (US); 1989.

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Webvision: The Organization of the Retina and Visual System [Internet].

Kolb H, Fernandez E, Nelson R, editors.

Salt Lake City (UT): University of Utah Health Sciences Center; 1995-.

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Opportunities in Biology.

National Research Council (US) Committee on Research Opportunities in Biology.

Washington (DC): National Academies Press (US); 1989.

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Retroviruses.

Coffin JM, Hughes SH, Varmus HE, editors.

Cold Spring Harbor (NY): Cold Spring Harbor Laboratory Press; 1997.

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Treatment for metastatic colorectal cancer in the liver amenable to treatment with curative intent: Colorectal cancer (update): Evidence review D2a.

National Guideline Alliance (UK).

London: National Institute for Health and Care Excellence (NICE); 2020 Jan. (NICE Guideline, No. 151.)

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Figure 2.17The alternative pathway of complement activation can amplify the classical or the MB-lectin pathway by forming an alternative C3 convertase and depositing more C3b molecules on the pathogen

C3b deposited by the classical or MB-lectin pathways can bind factor B, making it susceptible to cleavage by factor D. The C3b,Bb complex is the C3 convertase of the alternative pathway of complement activation and its action, like that of C4b,2b, results in the deposition of many molecules of C3b on the pathogen surface.

The complement system and innate immunity.

Janeway CA Jr, Travers P, Walport M, et al. Immunobiology: The Immune System in Health and Disease. 5th edition. New York: Garland Science; 2001.
Figure 2.7Schematic overview of the complement cascade

There are three pathways of complement activation: the classical pathway, which is triggered by antibody or by direct binding of complement component C1q to the pathogen surface; the MB-lectin pathway, which is triggered by mannan-binding lectin, a normal serum constituent that binds some encapsulated bacteria; and the alternative pathway, which is triggered directly on pathogen surfaces. All of these pathways generate a crucial enzymatic activity that, in turn, generates the effector molecules of complement. The three main consequences of complement activation are opsonization of pathogens, the recruitment of inflammatory cells, and direct killing of pathogens.

The complement system and innate immunity.

Janeway CA Jr, Travers P, Walport M, et al. Immunobiology: The Immune System in Health and Disease. 5th edition. New York: Garland Science; 2001.
Figure 2.12The proteins of the classical pathway of complement activation

The complement system and innate immunity.

Janeway CA Jr, Travers P, Walport M, et al. Immunobiology: The Immune System in Health and Disease. 5th edition. New York: Garland Science; 2001.
Figure 2.19Complement component C5 is cleaved when captured by a C3b molecule that is part of a C5 convertase complex

As shown in the top panel, C5 convertases are formed when C3b binds either the classical or MB-lectin pathway C3 convertase C4b,2b to form C4b,2b,3b, or the alternative pathway C3 convertase C3b,Bb to form C3b₂,Bb. C5 binds to the C3b in these complexes (center panel). The bottom panel shows how C5 is cleaved by the active enzyme C2b or Bb to form C5b and the inflammatory mediator C5a. Unlike C3b and C4b, C5b is not covalently bound to the cell surface. The production of C5b initiates the assembly of the terminal complement components.

The complement system and innate immunity.

Janeway CA Jr, Travers P, Walport M, et al. Immunobiology: The Immune System in Health and Disease. 5th edition. New York: Garland Science; 2001.