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.

We sought to determine whether the protective role of the 'obesity paradox' was present among elderly obese patients undergoing coronary artery bypass grafting (CABG) by median sternotomy. We retrospectively analyzed 1909 consecutive patients who underwent heart surgery between January 2006 and June 2009, and identified 396 patients who were ≥ 70 years of age and had isolated CABG. Subjects were divided into three groups according to their body mass index (BMI): obese (BMI ≥ 30 kg/m(2)), overweight (BMI 25-29.99 kg/m(2)) and normal (BMI 18.5-24.99 kg/m(2)). Of the 396 patients, 94 were obese, 167 were overweight, and 135 had a normal BMI. The composite of in-hospital complications and hospital mortality did not differ between the groups. Re-exploration for bleeding was required in none of the obese patients, which was statistically significant (P=0.05) compared to the other groups; otherwise there was no statistical difference for all other complications, including total length hospital stay and length of stay in the intensive care unit. Despite being labeled as higher risk candidates preoperatively, obese elderly patients undergoing CABG did not demonstrate an increased risk of postsurgical complications. We conclude that the 'obesity paradox' is present in this population, and they should not be excluded from receiving the benefits of CABG.

Staged PCI with minimally invasive valve surgery may offer an alternative to coronary bypass grafting with concurrent valve surgery and should be tested prospectively.

Soluble factors released from platelets can modulate the immune response of leukocytes. We and others have recently found that T lymphocytes with bound platelets have reduced proliferation and IFN-γ and IL-17 production. Thus, we speculate that if we induce the binding of platelets to lymphocytes, we will be able to regulate the inflammatory response. When we cocultured platelets with lymphocytes at different ratios, we were able to increase the percentage of lymphocytes with bound platelets. The coculture of platelets with lymphocytes in the presence of stimulation decreased the production of IFN-γ and TNF-α, T cell proliferation, and the expression of CD25, PD-L1, and SLAM. However, this coculture increased CD39 expression. All of these effects were dependent on the dose of platelets and operated indistinctly with platelets from different healthy donors. When platelets were cocultured in the same compartment with lymphocytes, we observed less IFN-γ and TNF-α production and T lymphocyte proliferation than in cultures with platelets separated from lymphocytes by a 0.4-μm pore size filter. The binding of platelets to lymphocytes was blocked with anti-P-selectin Abs, and when this occurred we observed higher IFN-γ and TNF-α production than in nonblocked conditions. The cocultures of platelets with synovial fluid cells from rheumatoid arthritis patients reduced inflammatory cytokine production and increased IL-10 production. These results suggest that platelet binding to lymphocytes effectively regulates T lymphocyte function. This mechanism could be easily applied to reduce inflammatory responses.

No abstract