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The number and activity of T cell subsets in the atherosclerotic plaques are critical for the prognosis of patients with acute coronary syndrome. β 2 Integrin activation is pivotal for T cell recruitment and correlates with future cardiac events. Despite this knowledge, differential regulation of adhesiveness in T cell subsets has not been explored yet. In this study, we show that in human T cells, SDF-1α-mediated β 2 integrin activation is driven by a, so far, not-described reactive oxidative species (ROS)-regulated calcium influx. Furthermore, we show that CD4 + CD28 null T cells represent a highly reactive subset showing 25-fold stronger β 2 integrin activation upon SDF-1α stimulation compared with CD28 + T cells. Interestingly, ROS-dependent Ca release was much more prevalent in the pathogenetically pivotal CD28 null subset compared with the CD28 + T cells, whereas the established mediators of the classical pathways for β 2 integrin activation (PKC, PI3K, and PLC) were similarly activated in both T cell subsets. Thus, interference with the calcium flux attenuates spontaneous adhesion of CD28 null T cells from acute coronary syndrome patients, and calcium ionophores abolished the observed differences in the adhesion properties between CD28 + and CD28 null T cells. Likewise, the adhesion of these T cell subsets was indistinguishable in the presence of exogenous ROS/H 2 O 2 Together, these data provide a molecular explanation of the role of ROS in pathogenesis of plaque destabilization.

Reactive Oxidative Species–Modulated Ca2+ Release Regulates β2 Integrin Activation on CD4+ CD28null T Cells of Acute Coronary Syndrome Patients