Functional consequences of platelet binding to T lymphocytes in inflammation

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. 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.