The complement system

Sarma, J. Vidya; Ward, Peter A

doi:10.1007/s00441-010-1034-0

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The complement system

review-article

Author(s): J. Vidya Sarma , Peter A. Ward

Publication date (Electronic): 14 September 2010

Journal: Cell and Tissue Research

Publisher: Springer-Verlag

Keywords: Complement, Activation pathways, Anaphylatoxins

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Abstract

The complement system consists of a tightly regulated network of proteins that play an important role in host defense and inflammation. Complement activation results in opsonization of pathogens and their removal by phagocytes, as well as cell lysis. Inappropriate complement activation and complement deficiencies are the underlying cause of the pathophysiology of many diseases such as systemic lupus erythematosus and asthma. This review represents an overview of the complement system in an effort to understand the beneficial as well as harmful roles it plays during inflammatory responses.

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Most cited references 49

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An integrated view of humoral innate immunity: pentraxins as a paradigm.

Barbara Bottazzi, Andrea Doni, Cecilia Garlanda … (2010)

The innate immune system consists of a cellular and a humoral arm. Pentraxins (e.g., the short pentraxin C reactive protein and the long pentraxin PTX3) are key components of the humoral arm of innate immunity which also includes complement components, collectins, and ficolins. In response to microorganisms and tissue damage, neutrophils, macrophages, and dendritic cells are major sources of fluid-phase pattern-recognition molecules (PRMs) belonging to different molecular classes. Humoral PRMs in turn interact with and regulate cellular effectors. Effector mechanisms of the humoral innate immune system include activation and regulation of the complement cascade; agglutination and neutralization; facilitation of recognition via cellular receptors (opsonization); and regulation of inflammation. Thus, the humoral arm of innate immunity is an integrated system consisting of different molecules and sharing functional outputs with antibodies.

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Complement-targeted therapeutics.

Daniel Ricklin, John D Lambris (2007)

The complement system is a central component of innate immunity and bridges the innate to the adaptive immune response. However, it can also turn its destructive capabilities against host cells and is involved in numerous diseases and pathological conditions. Modulation of the complement system has been recognized as a promising strategy in drug discovery, and a large number of therapeutic modalities have been developed. However, successful marketing of complement-targeted drugs has proved to be more difficult than initially expected, and many strategies have been discontinued. The US Food and Drug Administration's approval of the first complement-specific drug, an antibody against complement component C5 (eculizumab; Soliris), in March 2007, was a long-awaited breakthrough in the field. Approval of eculizumab validates the complement system as therapeutic target and might facilitate clinical development of other promising drug candidates.

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Viral subversion of the immune system.

Benjamin E. Gewurz, D Tortorella, Joseph Furman … (1999)

This review describes the diverse array of pathways and molecular targets that are used by viruses to elude immune detection and destruction. These include targeting of pathways for major histocompatibility complex-restricted antigen presentation, apoptosis, cytokine-mediated signaling, and humoral immune responses. The continuous interactions between host and pathogens during their coevolution have shaped the immune system, but also the counter measures used by pathogens. Further study of their interactions should improve our ability to manipulate and exploit the various pathogens.

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Author and article information

Contributors

Peter A. Ward: +1-734-6472921 , +1-734-7644308 , pward@umich.edu

Journal

Journal ID (nlm-ta): Cell Tissue Res

Journal ID (iso-abbrev): Cell Tissue Res

Title: Cell and Tissue Research

Publisher: Springer-Verlag (Berlin/Heidelberg )

ISSN (Print): 0302-766X

ISSN (Electronic): 1432-0878

Publication date (Electronic): 14 September 2010

Publication date (Print): 2011

Volume: 343

Issue: 1

Pages: 227-235

Affiliations

GRID grid.214458.e, ISNI 0000000086837370, Department of Pathology, , The University of Michigan Medical School, ; 1301 Catherine Rd., Box 5602, Ann Arbor, MI 48109-5602 USA

Article

Publisher ID: 1034

DOI: 10.1007/s00441-010-1034-0

PMC ID: 3097465

PubMed ID: 20838815

SO-VID: 457c4c1e-519a-4c97-ba46-457e0219e954

License:

This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.