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C-reactive protein and C1q regulate platelet adhesion and activation on adsorbed immunoglobulin G and albumin
Department of Physics, Chemistry and Biology, Materials in Medicine, Division of Applied Physics, Linköping University, Linköping, Sweden; Department of Medical Sciences, Cardiovascular Inflammation Research Center, Linköping University, Linköping, Sweden; Department of Medical Sciences, Division of Pharmacology, Linköping University, Linköping, Sweden.
Department of Clinical and Experimental Medicine, Division of Rheumatology/Autoimmunity and Immune Regulation Unit, Linköping University, Linköping, Sweden.
Department of Clinical and Experimental Medicine, Division of Rheumatology/Autoimmunity and Immune Regulation Unit, Linköping University, Linköping, Sweden.
Department of Clinical and Experimental Medicine, Division of Rheumatology/Autoimmunity and Immune Regulation Unit, Linköping University, Linköping, Sweden.
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2008 (English)In: Immunology and Cell Biology, ISSN 0818-9641, E-ISSN 1440-1711, Vol. 86, no 5, 466-474 p.Article in journal (Refereed) Published
Abstract [en]

Blood platelets and C-reactive protein (CRP) are both used clinically as markers of ongoing inflammation, and both participate actively in inflammatory responses, although the biological effects are still incompletely understood. Rapidly adhering platelets express receptors for complement factor 1q (C1q) and the Fc part of immunoglobulin G (IgG), and CRP is known to activate/regulate complement via C1q binding, and to ligate FcgammaRs. In the present study, we used normal human IgG pre-adsorbed to a well-characterized methylated surface as a model solid-phase immune complex when investigating the effects of CRP and C1q on platelet adhesion and activation. Protein adsorption was characterized using ellipsometry and polyclonal antibodies, and human serum albumin (HSA) and non-coated surfaces were used as reference surfaces. Platelet adhesion to IgG and HSA was inhibited by both C1q and CRP. Furthermore, CRP (moderately) and C1q (markedly) decreased the spreading of adhering platelets. The combination of C1q and CRP was slightly more potent in reducing cell adhesion to IgG, and also impaired the adhesion to HSA and non-coated surfaces. Platelet production of thromboxane B2 (TXB(2)) was also reduced by C1q both in the presence and absence of CRP, whereas CRP alone had no effect on TXB(2) production. We conclude that CRP and C1q regulate the behaviour of platelets, and that this may be an important immunoregulatory mechanism during inflammatory conditions.

Place, publisher, year, edition, pages
Nature Publishing Group, 2008. Vol. 86, no 5, 466-474 p.
Keyword [en]
acute-phase response; C-reactive protein (CRP); complement; inflammation; plasma protein adsorption; platelets
National Category
Cell and Molecular Biology Immunology in the medical area
Identifiers
URN: urn:nbn:se:oru:diva-56664DOI: 10.1038/icb.2008.9ISI: 000257634100012PubMedID: 18332893Scopus ID: 2-s2.0-46749083444OAI: oai:DiVA.org:oru-56664DiVA: diva2:1083519
Available from: 2017-03-21 Created: 2017-03-21 Last updated: 2017-10-18Bibliographically approved

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