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- Hamad, Osama A.,1978-Uppsala universitet,Enheten för klinisk immunologi,Complement And Biomaterials (author)
Non-proteolytically activated C3 promotes binding of activated platelets and platelet-derived microparticles to leukocytes via CD11b/CD18
- Article/chapterEnglish2012
Publisher, publication year, extent ...
- Elsevier BV,2012
- printrdacarrier
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- LIBRIS-ID:oai:DiVA.org:uu-123624
- https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-123624URI
- https://doi.org/10.1016/j.imbio.2012.08.178DOI
- https://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-23355URI
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- Language:English
- Summary in:English
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Notes
- Background:We have previously demonstrated that complement component C3 binds to the surface of activated platelets, independent of proteolytic activation. The resulting form of C3, termed C3(H2O), was shown to be a ligand for recombinant CD35 (complement receptor 1, CR1). Previous studies by others have indicated that platelet-leukocyte complex (PLC) formation is dependent on the interaction between platelet exposed P-selectin (CD62P) and its ligand, PSGL-1, on leukocytes. In addition, CD11b/CD18 (Mac-1 or CR3) has been shown to participate in this reaction, but its ligand has not yet been identified.Objective:To test the hypothesis that C3 bound to activated platelets and platelet-derived microparticles (PMPs) can act as a ligand for CD11b/CD18 (CR3) and contribute to PLC formation.Methods and results:Blood cells were depleted of plasma proteins. After extensive washing, C3 was added, and the leukocytes were activated with C5a and the platelets with thrombin receptor-activating peptide (TRAP). PLC formation was detected by flow cytometry (monocytes: CD14+/CD42a+, granulocytes: CD16+/CD42a+). For both granulocytes and monocytes, the addition of C3 significantly enhanced PLC formation. Formation of PLC was inhibited by both anti-P-selectin and anti-CD11b monoclonal antibodies. In addition, PMPs isolated from serum, were found to expose C3(H2O) and bind to leukocytes in a fashion similar to activated platelets.Conclusion:We have identified proteolytically non-activated C3 as a ligand for CD11b in the formation of PLC and possibly the binding of PMPs to leukocytes. This observation most likely has pathophysiological implications for the recently reported links between thrombotic disease and the complement system.
Subject headings and genre
- 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
- NATURVETENSKAP Biologi Immunologi hsv//swe
- NATURAL SCIENCES Biological Sciences Immunology hsv//eng
- platelet activation
- complement
- platelet-leukocyte complexes
- PMP
- CD11b/CD18
- complement component 3
- Immunology
- Immunologi
- Klinisk immunologi
- Clinical Immunology
- Immunologi
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- Nilsson Ekdahl, KristinaLinnéuniversitetet,Institutionen för naturvetenskap, NV(Swepub:lnu)nnikr (author)
- Nilsson, BoUppsala universitet,Klinisk immunologi(Swepub:uu)bonils (author)
- Uppsala universitetEnheten för klinisk immunologi (creator_code:org_t)
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- In:Immunobiology: Elsevier BV217:11, s. 1191-11910171-29851878-3279
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