Regulatory T cells and IL-10 levels are reduced in patients with vulnerable coronary plaques

BackgroundDespite having a similar large extent of atherosclerotic coronary affliction, some patients suffer of recurrent cardiac events, whereas others remain asymptomatic.HypothesisWe hypothesized the existence of a systemic “signature” that could distinguish “vulnerable” patients with preexisting coronary atherosclerosis from those having similar risk factors and atheromatous burden, but no history of clinically evident plaque rupture/erosion.MethodsTwenty three patients who had at least two prior myocardial infarctions (“vulnerable group”) were matched in respect to their background and coronary atherosclerosis extent with twenty one patients without a history of previous myocardial infarction who underwent routine coronary angiography before valvular surgery. We studied a panel of cytokines, antibodies and hormones including IL-6, IL-10, IL-12, antibodies to β2 glycoprotein I (β2GPI), antibodies to oxidized-LDL, adiponectin and resistin, along with levels of circulating EPCs and Tregs.ResultsA significantly higher level of Treg cells was present in the control (73.4% ± 4) than in the “vulnerable patient” group (62.2% ± 10.7), p < 0.001. IL-10 level was also significantly higher in the control than in the vulnerable patients (2.6 ± 1.2 pg/ml versus 0.9 ± 0.1 pg/ml respectively, p = 0.03). There was no significant difference in the circulating levels of the other cytokines, hormones or EPCs between the two groups.ConclusionRegulatory T cells and serum IL-10 may discriminate “vulnerable” versus stable patients and may have a protective role against plaque rupture in patients with coronary atherosclerosis.

► Patients with stable atherosclerotic plaques have a higher level of Tregs and IL-10 than vulnerable patients. ► We found no difference in other chemokines studied between the two patient groups. ► We found no difference in EPCs, antibodies to β2GPI, antibodies to ox-LDL, adiponectin or resistin between the two groups.