Abstract

The frequency and profile of lymphocyte subsets within the culprit coronary artery were investigated in 33 patients with myocardial infarction and compared to their systemic circulating counterparts. T cell subsets including CD4+CD28null, activated and regulatory T-cells, TH1/TH2/TH17 phenotypes, NK and B-cells were studied in intracoronary (IC) and arterial peripheral blood (PB) samples. CD4+CD28null T-lymphocytes were significantly increased in IC compared to PB (3.7 vs. 2.9 %, p < 0.0001). Moreover, patients with more than 6 h of evolution of STEMI exhibited higher levels of CD4+CD28null T-cells suggesting that this subset may be associated with more intense myocardial damage. The rare NK subpopulation CD3−CD16+CD56− was also increased in IC samples (5.6 vs. 3.9 %, p = 0.006). CD4+CD28null T-cells and CD3−CD16+CD56− NK subpopulations were also associated with higher CK levels. Additionally, IFN-γ and IL10 were significantly higher in IC CD4+ lymphocytes. Particular immune cell populations with a pro-inflammatory profile at the site of onset were increased relative to their circulating counterparts suggesting a pathophysiological role of these cells in plaque instability, thrombi and myocardial damage.

Highlights

  • Atherosclerosis is regarded as a chronic inflammatory disease of the arterial wall (Hansson 2005)

  • Lymphocyte subsets in intracoronary and arterial peripheral blood T cells No differences were found in total T cell frequency among the IC and PB samples (Table 2)

  • The frequencies of CD3+CD4+IFN-γ+ and CD3+CD4+IL-10 + cells were significantly higher in IC blood. (p = 0.005 and p = 0.014, respectively, Wilcoxon signed rank test) we investigated different lymphocyte subsets and intracellular cytokine production in intracoronary blood of patients with ST-segment elevation myocardial infarction (STEMI) and compare them with their PB counterparts

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Summary

Introduction

Atherosclerosis is regarded as a chronic inflammatory disease of the arterial wall (Hansson 2005). Postmortem studies showed that this CD4+ subset accumulates preferentially in ruptured plaques and produces high levels of Interferon-gamma (IFN-γ) (Eid et al 2009; Giubilato et al 2011; Liuzzo et al 2000). Detailed analysis of CD4+ T-cells in acute coronary syndromes (ACS) revealed the expansion in peripheral blood of an unusual subset (Morishita et al 1989), that does not express the co-estimulatory receptor CD28 (CD4+CD28null) (Liuzzo et al 1999) (Zal et al 2008). Reduction of natural killer (NK) and regulatory T-cells (Tregs) are linked to atherosclerosis (Jonasson et al 2005; Han et al 2007; Sardella et al 2007). Ammirati et al showed that Tregs were increased in STEMI compared with non-ST- elevation ACS (Ammirati et al 2010)

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