It was shown previously to recruit NK cells in an atherosclerotic plaque [11]. Therefore, it is likely that IL-15 plays an important role in the recruitment of activated leucocytes from the blood stream in the infracted myocardial region of persons who died early after MAPK inhibitor an acute coronary event. This hypothesis is supported by the abundant IL-15 expression in the border-necrotic, viable myocardiocytes that surround lymphocytes infiltration in the form of necklace. Although the CD56+bright NK cell subset represents mostly

cytokine-producing, regulatory NK cells in a steady state condition, they are able to become highly cytotoxic under tissue-specific inflammatory Th1 cytokine stimulation, such as the combination of IL-15 with other cytokines [12]. This was confirmed in vitro even with decidual CD56+bright NK cells [27], whose cytotoxicity is normally strongly down-regulated in situ by local immune-endocrine interactions during the first trimester of pregnancy. However, there is no clear evidence for JAK inhibitor the involvement of particular cytotoxic mediator(s) in the

apoptosis of myocardial tissue after infarction. Here, we show for the first time the presence of the pro-apoptotic molecule GNLY in the cytoplasm of CD3+ and CD56+ cells, which take part in lymphocyte infiltration in the centre of MI in the patients who died in the first week after coronary artery thrombosis. GNLY can be easily released from the cells upon pro-inflammatory stimulation [19], what is supported with significantly lower MFI for GNLY in peripheral blood

lymphocytes of MI patients when compared with healthy control. NADPH-cytochrome-c2 reductase In turn, the soluble mature form of GNLY could enhance secretion of Th1 chemokines from macrophages and exhibit chemotactic properties for monocytes, mature dendritic cells, NK cells, and CD4+ and CD8+ T cells with a CD45RO+ phenotype, but not naïve CD45RA+ cells, as was shown previously [19], thus contributing to the accumulation of immune effectors in the myocardium after infarction [2]. On the other side, GNLY could hasten resolution rather than worsen cardiac post-infarction inflammation because of the finding of GNLY+ cells within accumulations of apoptotic leucocytes 1 week after the acute coronary event. K562 killing represents a model for in vitro testing of NK cell-mediated self-aggression, because K562 cells do not express MHC class I protein forms, as is known for damaged tissue cells [30]. Significant spontaneous peripheral blood NK cell- and GNLY-mediated apoptosis of K562 cells, which occurs in the first week after the acute coronary event, disappeared on day 14, with a concomitant decrease in the percentage of GNLY+ cells and the GNLY+ CD56+ bright NK cell subset in the circulation.