Journal
THROMBOSIS AND HAEMOSTASIS
Volume 106, Issue 2, Pages 353-362Publisher
GEORG THIEME VERLAG KG
DOI: 10.1160/TH11-01-0020
Keywords
Platelets; CD4(+) T cells; regulatory T cells; T(H)17 cells; adaptive immunity
Categories
Funding
- Swedish Research Council
- Swedish Heart-Lung Foundation
- Karolinska Institute
- Swedish Society of Medicine
- Stockholm County Council
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Atherosclerosis is an inflammatory and thrombotic disease. Both platelets and lymphocytes play important roles in atherogenesis. However, information on their interaction is limited. We therefore studied how platelets regulate CD4(+) T cell activation and differentiation. Human CD4(+) T cells and autologous platelets were co-cultured. Platelets concentration-dependently enhanced anti-CD3/CD28-induced IFN gamma production by CD4(+) T cells, but attenuated their proliferation. Abrogation of heterotypic cell-cell contact partially reversed the enhancement, and supernatant from activated platelets partially mimicked the enhancement, suggesting that platelets exert their effects via both soluble mediators and direct cell-cell contact. Platelets enhanced the production of IL-10 and cytokines characteristic for type 1 T helper (T(H)1) (IFN gamma/TNF alpha) and T(H)17 (IL-17) cells, but influenced T(H)2 cytokines (IL-4/IL-5) little. The cytokine responses were accompanied by enhanced T(H)1/T(H)17/T-Reg differentiation. Using neutralising antibodies and recombinant PF4, RANTES, and TGF beta, we found that platelet-derived PF4 and RANTES enhanced both pro- and anti-inflammatory cytokine production, whilst recombinant TGF beta enhanced IL-10 but not TNF alpha production. In conclusion, platelets enhance the differentiation and cytokine production of anti-CD3/CD28-stimulated CD4(+) T cells via both multiple chemokines and direct cell-cell contact. Our study provides new insights into the cross-talk between thrombosis and adaptive immunity, and indicates that platelets can enhance T-effector cell development.
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