Crosstalk Between Activated Platelets and the Complement System

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Hamad, Osama A.,1978-Uppsala universitet,Enheten för klinisk immunologi,Complement And Biomaterial (författare)

Crosstalk Between Activated Platelets and the Complement System

BokEngelska2010

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Uppsala :Acta Universitatis Upsaliensis,2010
82 s.
electronicrdacarrier

Nummerbeteckningar

LIBRIS-ID:oai:DiVA.org:uu-123681
ISBN:9789155478223
https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-123681URI

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Språk:engelska
Sammanfattning på:engelska

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Ämneskategori:dok swepub-publicationtype

Anmärkningar

Several studies have shown that complement and thrombotic events co-exist. Platelets have been suspected to act as the bridge between the two cascade systems. To study the platelet-induced complement activation we developed a system in which platelets were activated by thrombin receptor activating peptide (TRAP) in platelet rich plasma (PRP) or whole blood anti-coagulated using the specific thrombin inhibitor, lepirudin. TRAP-activated platelets induced a fluid-phase complement activation measured as generation of C3a and sC5b-9, triggered by released chondroitin sulphate-A (CS-A) which interacted with C1q and activated the complement system through the classical pathway. Complement components C1q, C3, C4 and C9 were also shown to bind to TRAP-activated platelets but this binding did not seem to be due to a complement activation since blocking of complement activation at the C1q or C3 levels did not affect the binding of the complement proteins. The C3 which bound to activated platelets consisted of C3(H2O), indicating that bound C3 was not proteolytically activated. Binding of C1q was partially dependent on CS-A exposure on activated platelets. The abolished complement activation on the surface of activated platelets was suggested to be dependent on the involvement of several complement inhibitors. We confirmed the binding of C1INH and factor H to activated platelets. To this list we have added another potent complement inhibitor, C4BP. The binding of factor H and C4BP was shown to be dependent on exposure of CS-A on activated platelets. The physiological relevance of these reactions was reflected in an elevated expression of CD11b on leukocytes, and increased generation of platelet-leukocyte complexes. The platelets were involved in these events by at least two different mechanisms; generation of C5a which activated leukocytes and binding of C3(H2O)/iC3(H2O), a ligand to the intergrin CD11b/CD18 on their surface. These mechanisms add further to the understanding of how platelets interact with the complement system and will help us to understand the role of the complement system in cardiovascular disease and thrombotic conditions.

Ämnesord och genrebeteckningar

MEDICIN OCH HÄLSOVETENSKAP Medicinska och farmaceutiska grundvetenskaper Immunologi inom det medicinska området hsv//swe
MEDICAL AND HEALTH SCIENCES Basic Medicine Immunology in the Medical Area hsv//eng
platelets
activated platelets
TRAP
chondroitin sulfate
C1q
factor H
C4BP
C3
Compstatin
complement
platelet-leukocyte complexes
platelet microparticles
Clinical immunology
Klinisk immunologi
Klinisk immunologi
Clinical Immunology

Biuppslag (personer, institutioner, konferenser, titlar ...)

Nilsson, Bo,ProfessorUppsala universitet,Enheten för klinisk immunologi (preses)
Ekdahl-Nilsson, Kristina,ProfessorUppsala universitet,Enheten för klinisk immunologi (preses)
Truedsson, Lennart,ProfessorLunds Universitet, Institute of Laboratory Medicine (opponent)
Uppsala universitetEnheten för klinisk immunologi (creator_code:org_t)

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Av lärosätet: Uppsala universitet

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