Identification of unique adaptive immune system signature in acute coronary syndromes

Several studies have consistently demonstrated that inflammation plays a key role in the pathogenesis of acute coronary syndromes (ACS). More recent studies have highlighted the importance of adaptive immunity in ACS. In particular, profound abnormalities have been observed in specific subsets of T-cells, including CD4+CD28nullT-cells, a subset of cytotoxic CD4+T-lymphocytes producing large amount of interferon-γ (IFN-γ), naturally occurring regulatory T-cells (Treg)and interleukin (IL)-17-producing T-cells (Th17). Our group systematically investigated the clinical relevance of adaptive immunity alterations, in a sizeable population of patients with non-ST elevation (NSTE)-ACS (n = 95), as compared with patients presenting chronic stable angina (SA) (n = 80) and individuals without overt cardiovascular diseases (controls) (n = 70). Our data show for the first time that about half of patients with ACS exhibit a unique immune profile, associated with a worse outcome at 1-year follow-up, which is very rarely found in SA and never in healthy controls. In this subset of ACS patients, the failure to mount a counter regulatory response to the activation of aggressive T-cells might play a key pathogenetic role and might represent an attractive therapeutic target [17]. The remaining half of ACS patients consisted of a small subset with an immune profile similar to that found in SA and in controls, and of a larger subset exhibiting a heterogeneous immune profile. In these subsets, coronary instability is unlikely to be caused by an inflammatory outburst.