Journal
JOURNAL OF IMMUNOLOGY
Volume 172, Issue 4, Pages 2011-2015Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.172.4.2011
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Funding
- NIAID NIH HHS [AI53188] Funding Source: Medline
- NIDDK NIH HHS [DK30399, DK50984] Funding Source: Medline
- NIGMS NIH HHS [F31 GM66499] Funding Source: Medline
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Platelets, in addition to exerting hemostatic activity, contribute to immunity and inflammation. The recent report that platelets express CD40 led us to hypothesize that CD40 ligand (CD40L)-positive T cells could bind to platelets, cause their activation, and trigger granular RANTES release, creating a T cell recruitment feedback loop. Platelets were cocultured with resting or activated autologous T cells and their activation was assessed by P-selectin expression. RANTES binding to endothelial cells was assessed by confocal microscopy, and its biological activity was demonstrated by a T cell adbesion assay. CD40L-positive T cells induced platelet activation through a contact-mediated, CD40-dependent pathway resulting in RANTES release, which bound to endothelial cells and mediated T cell recruitment. Soluble CD40L induced the same events via p38, but not extracellular signal-regulated kinase, phosphorylation. These results show the existence of a novel platelet-dependent pathway of immune response amplification which brings these nonimmune cells close to the level of pathogenic relevance traditionally attributed to classical immune cells.
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