Effect of Coronary Percutaneous Revascularization on Interferon-γ and Interleukin-10 Producing CD4 + T Cells during Acute Myocardial Infarction

T lymphocytes play an important role in the induction and progression of acute coronary syndromes (ACS). To gain insight into how different T cell subsets can influence ACS, we analyzed the frequencies of circulating CD4⁺T cells producing either pro-inflammatory interferon(IFN)-γ or anti-inflammatory interleukin (IL)-10 in subjects presenting with ST-elevation myocardial infarction (STEMI). The effect of coronary bare metal (BS) and paclitaxel-eluting stent (PES) on the balance between CD4⁺IFN-γ⁺ and CD4⁺IL-10⁺ lymphocytes was also investigated. Peripheral blood mononuclear cells (PBMC) were isolated from 38 consecutive patients with STEMI before and 48 hrs or 6 days after implantation of either BS or PES. Twenty patients with no history of coronary artery disease were included as basal controls. PBMC were stimulated in vitro with anti-CD3/anti-CD28 monoclonal antibodies, and CD4⁺IFN-γ⁺ or CD4⁺IL-10⁺ T cells were detected by flow cytometry intracellular staining. The frequency of peripheral CD4⁺IL-10⁺ T cells was significantly higher in STEMI patients as compared with controls. Conversely, the frequency of CD4⁺IFN-γ⁺ T lymphocytes did not differ between STEMI and subjects without history of coronary artery disease. Six days after the revascularization procedure, the percentage of CD4⁺IL-10⁺ T cells was significantly decreased in BS but not in the PES group, whereas the relative percentage of CD4⁺IFN-γ⁺ T lymphocytes were diminished in both groups as compared with baseline levels. Our data indicate that STEMI is associated with a peripheral expansion of CD4⁺IL-10⁺T lymphocytes, and that primary coronary revascularization with implantation of either BS or PES is followed by a reduction in circulating CD4⁺IFN-γ⁺ T lymphocytes. PES implantation, however, appears to inhibit the relative decrease of the IL-10 producing lymphocyte as observed in BS implanted patients, shifting the balance between pro-inflammatory and anti-inflammatory T cell populations in favor of the latter.