Functional consequences of platelet binding to T lymphocytes in inflammation. Issue 3 (25th June 2013)

• Record Type: Journal Article
• Authors: Zamora, Carlos; Cantó, Elisabet; Nieto, Juan C.; Ortiz, M. Angels; Diaz‐Torné, Cesar; Diaz‐Lopez, Cesar; Llobet, Josep M.; Juarez, Candido; Vidal, Sílvia
• Is Part Of: Journal of leukocyte biology. Volume 94:Issue 3(2013)
• Page Start: 521
• Page End: 529
• Publication Date: 2013-06-25
• Subjects: human -- T cell activation -- rheumatoid arthritis; Leucocytes -- Periodicals; Reticulo-endothelial system -- Periodicals; 571.96
• DOI: 10.1189/jlb.0213074
• Languages: English
• ISSNs: 0741-5400

Abstract

Abstract : Platelet binding is a new regulatory mechanism of T cell function; higher frequency of platelet binding to lymphocytes is associated with low severe inflammatory profile. Abstract : Expression of the scavenger receptor CD36 on lymphocytes is intriguing. We observed that a minor subpopulation of lymphocytes expressed CD36 on the cell surface. We investigated the source of CD36 and also the proliferation and cytokine production of these CD36 + CD4 + lymphocytes. Flow cytometry analysis and immunofluorescence microscopy showed that CD36 + platelets were responsible for CD36 detection on lymphocytes. CD36 was then used as a tool to characterize lymphocytes with bound platelets. Activation‐induced proliferation was lower in CD4 + lymphocytes with bound platelets than lymphocytes without bound platelets. IL‐17 and IFN‐γ production was also reduced in lymphocytes with bound platelets. We then studied the presence of CD36 + CD4 + lymphocytes in RA patients. We observed that the percentage of CD4 + lymphocytes with bound platelets was higher on RA patients than in healthy donors. RA patients with higher titers of anti‐CCP, RF levels, and cardiovascular risk index presented a lower percentage of CD4 + lymphocytes with bound platelets. These patients also had higher IL‐17 and IFN‐γ production. These results suggest that platelet‐binding modifies lymphocyte function. This binding could be a regulatory mechanism in RA that confers a less severe phenotype.