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Toll‐like receptor 4 ligand can differentially modulate the release of cytokines by human platelets
Author(s) -
Cognasse Fabrice,
HamzehCognasse Hind,
Lafarge Sandrine,
Delezay Olivier,
Pozzetto Bruno,
McNicol Archie,
Garraud Olivier
Publication year - 2008
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2008.06999.x
Subject(s) - platelet , angiogenin , tlr4 , platelet activation , cytokine , receptor , toll like receptor , monoclonal antibody , lipopolysaccharide , growth factor , chemistry , platelet derived growth factor receptor , biology , microbiology and biotechnology , immunology , biochemistry , antibody , cancer research , innate immune system , angiogenesis
Summary Blood platelets link the processes of haemostasis and inflammation. This study examined the immunomodulatory factors released by platelets after Toll‐Like Receptor 4 (TLR4) engagement on their surfaces. Monoclonal anti‐human FcγRII Ab (IV.3)‐treated human platelets were cultured with TLR4 ligands in the presence or absence of blocking monoclonal antibody to human TLR4. The release of sCD62p, epidermal growth factor (EGF), transforming growth factor β (TGFβ), interleukin (IL)‐8, platelet activating factor 4 (PAF4), platelet‐derived growth factor, α, β polypeptide (PDGF‐AB), Angiogenin, RANTES (regulated upon activation, normal T‐cell expressed, and presumably secreted) and sCD40L were measured by specific enzyme‐linked immunosorbent assay. TLR4 ligand [ Escherichia coli lipopolysaccharide (LPS)] bound platelet TLR4, which differentially modulates the release of cytokines by platelets. It was noted that (i) sCD62p, IL‐8, EGF and TGFβ release were each independent of platelet activation after TLR4 engagement; (ii) RANTES, Angiogenin and PDGF‐AB concentration were weaker in platelet supernatant after TLR4 engagement; (iii) sCD40L and PAF4 are present in large concentration in the releaseate of platelets stimulated by TLR4 ligand. The effects of LPS from E. coli on the modulation of secretory factors were attenuated by preincubation of platelets with an anti‐TLR4 monoclonal antibody, consistent with the immunomodulation being specifically mediated by the TLR4 receptor. We propose that platelets adapt the subsequent responses, with polarized cytokine secretion, after TLR4 involvement.