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Pentraxins in Complement Activation and Regulation

The complement is the first line of immune defense system involved in elimination of invading pathogens and dying host cells. Its activation is mainly triggered by immune complexes or pattern recognition molecules (PRMs) upon recognition against non-self or altered self-cells, such as C1q, collectin...

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Autores principales: Ma, Ying Jie, Garred, Peter
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6305747/
https://www.ncbi.nlm.nih.gov/pubmed/30619374
http://dx.doi.org/10.3389/fimmu.2018.03046
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author Ma, Ying Jie
Garred, Peter
author_facet Ma, Ying Jie
Garred, Peter
author_sort Ma, Ying Jie
collection PubMed
description The complement is the first line of immune defense system involved in elimination of invading pathogens and dying host cells. Its activation is mainly triggered by immune complexes or pattern recognition molecules (PRMs) upon recognition against non-self or altered self-cells, such as C1q, collectins, ficolins, and properdin. Recent findings have interestingly shown that the pentraxins (C-reactive protein, CRP; serum-amyloid P component, SAP; long pentraxin 3, PTX3) are involved in complement activation and amplification via communication with complement initiation PRMs, but also complement regulation via recruitment of complement regulators, for instance C4b binding protein (C4BP) and factor H (fH). This review addresses the potential roles of the pentraxins in the complement system during infection and inflammation, and emphasizes the underlining implications of the pentraxins in the context of complement activation and regulation both under physiological and pathological conditions.
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spelling pubmed-63057472019-01-07 Pentraxins in Complement Activation and Regulation Ma, Ying Jie Garred, Peter Front Immunol Immunology The complement is the first line of immune defense system involved in elimination of invading pathogens and dying host cells. Its activation is mainly triggered by immune complexes or pattern recognition molecules (PRMs) upon recognition against non-self or altered self-cells, such as C1q, collectins, ficolins, and properdin. Recent findings have interestingly shown that the pentraxins (C-reactive protein, CRP; serum-amyloid P component, SAP; long pentraxin 3, PTX3) are involved in complement activation and amplification via communication with complement initiation PRMs, but also complement regulation via recruitment of complement regulators, for instance C4b binding protein (C4BP) and factor H (fH). This review addresses the potential roles of the pentraxins in the complement system during infection and inflammation, and emphasizes the underlining implications of the pentraxins in the context of complement activation and regulation both under physiological and pathological conditions. Frontiers Media S.A. 2018-12-19 /pmc/articles/PMC6305747/ /pubmed/30619374 http://dx.doi.org/10.3389/fimmu.2018.03046 Text en Copyright © 2018 Ma and Garred. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Ma, Ying Jie
Garred, Peter
Pentraxins in Complement Activation and Regulation
title Pentraxins in Complement Activation and Regulation
title_full Pentraxins in Complement Activation and Regulation
title_fullStr Pentraxins in Complement Activation and Regulation
title_full_unstemmed Pentraxins in Complement Activation and Regulation
title_short Pentraxins in Complement Activation and Regulation
title_sort pentraxins in complement activation and regulation
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6305747/
https://www.ncbi.nlm.nih.gov/pubmed/30619374
http://dx.doi.org/10.3389/fimmu.2018.03046
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