Level of circulating CD4+ 28null cells in chronic inflammatory diseases: an important marker in predicting acute coronary events?

Abstract

Emerging and established evidence in the last decade has clearly established that atherosclerosis is an inXammatory disease. InXammation not only plays an important role in the development of the atherosclerotic plaque but also in the rupture of the plaque leading to critical ischaemia [1]. There is an increasing interest in identifying the immunological mediators that play an important role in plaque rupture. A subset of CD4 T cells lacking the surface expression of CD28 (CD4+ 28 cells) has been identiWed as potential culprits in driving this process. CD4+ 28 cells are the type of lymphocytes not usually found in young individuals. They have been identiWed in the peripheral circulation of elderly individuals and in patients with chronic inXammatory diseases and they diVer from other T cells in their ability to resist apoptosis [2]. Interestingly, they are found in higher numbers in patients with acute coronary syndromes when compared with patients with stable angina [3] and their appearance is strongly associated with the recurrence of acute coronary events suggesting an important role in plaque rupture [4]. These cells are also identiWed in patients with rheumatoid arthritis (RA), Wegener’s granulomatosis and Crohn’s disease [5–7]. In patients with RA, their presence is signiWcantly associated not only with extraarticular features and severe joint destruction but also with preclinical atherosclerotic changes, including arterial endothelial dysfunction and carotid artery wall thickening [5, 8]. In contrast, although patients with primary Sjogren’s syndrome (PSS) have an increased incidence of subclinical atherosclerosis, there is no evidence that mortality due to cardiovascular events is increased [9, 10]. This might be due to the fact that in patients with PSS the number of CD4+ 28 cells in peripheral circulation is not high when compared with healthy controls [10]. Interestingly until now no research is done to look at the role of these cells in patients with systemic lupus erythematosus (SLE). In my opinion, monitoring the levels of these cells in patients with chronic inXammatory diseases will help in identifying an important group of patients who are at a very high risk of developing ischaemic events, thereby allowing aggressive modiWcation of cardiovascular risk factors and initiating further investigations and treatment. More studies are needed to look at the role of these very important T cells in the pathogenesis of atherosclerosis in SLE.