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Giuseppina Caligiuri, Antonino Nicoletti, Lymphocyte responses in acute coronary syndromes: lack of regulation spawns deviant behaviour
, European Heart Journal, Volume 27, Issue 21, November 2006, Pages 2485–2486, https://doi.org/10.1093/eurheartj/ehl284The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.
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The inflammatory and immune systems are abnormally activated during the acute phases of coronary atherosclerotic disease.1,2 In particular, an unusual population of effector cells, lacking costimulatory molecule CD28, is transiently expanded in parallel with the occurrence of the waxing phases of atherosclerotic coronary disease.3
The origin of the lymphocyte response in acute coronary syndromes has been a matter of debate in the last decade. Questions still overcome the answers. It has been demonstrated that the T-cell response can be directed to restricted antigens within the culprit lesions,4 and it was suggested that persistent antigenic stimulation could generate the unusual expansion of the aggressive CD28 negative effector cells that are characteristically expanded in autoimmune diseases such as rheumatoid arthritis.3 However, the putative target antigenic stimuli evoked in acute coronary syndromes can also be found in patients with chronic atherosclerotic disease. Indeed, self-reactive antibodies recognize similar antigenic epitopes in patients with acute or stable coronary syndromes and in the normal population.5 Altogether, these findings indicate that the repertoire of antigens targeted by the immune system cannot explain the deviant lymphocyte responses observed in acute coronary disease.
