BACKGROUND: To evaluate the activity of natural killer cells through their inhibitory and activating receptors and quantity in peripheral blood mononuclear cells extracted from patients with acute myocardial infarction, stable angina pectoris and the controls. METHODS: 100 patients with myocardial infarction, 100 with stable angina, and 20 healthy volunteers were recruited into the study. 20 randomly chosen people per group were examined for the whole human genome microarray analysis to detect the gene expressions of all 40 inhibitory and activating natural killer cell receptors. Flow cytometry analysis was applied to all 200 patients to measure the quantity of natural killer cells. RESULTS: In myocardial infarction group, the mRNA expressions of six inhibitory receptors KIR2DL2, KIR3DL3, CD94, NKG2A, KLRB1, KLRG1, and eight activating receptors KIR2DS3, KIR2DS5, NKp30, NTB-A, CRACC, CD2, CD7 and CD96 were significantly down-regulated (P<0.05) compared with both angina patients and the controls. There was no statistical difference in receptor expressions between angina patients and control group. The quantity of natural killer cells was significantly decreased in both infarction and angina patients compared with normal range (P<0.001). CONCLUSIONS: The significant mRNAs down-regulation of several receptors in myocardial infarction group and reduction in the quantity of natural killer cells in both myocardial infarction and angina patients showed a quantitative loss and dysfunction of natural killer cells in myocardial infarction patients.
BACKGROUND: To evaluate the activity of natural killer cells through their inhibitory and activating receptors and quantity in peripheral blood mononuclear cells extracted from patients with acute myocardial infarction, stable angina pectoris and the controls. METHODS: 100 patients with myocardial infarction, 100 with stable angina, and 20 healthy volunteers were recruited into the study. 20 randomly chosen people per group were examined for the whole human genome microarray analysis to detect the gene expressions of all 40 inhibitory and activating natural killer cell receptors. Flow cytometry analysis was applied to all 200 patients to measure the quantity of natural killer cells. RESULTS: In myocardial infarction group, the mRNA expressions of six inhibitory receptors KIR2DL2, KIR3DL3, CD94, NKG2A, KLRB1, KLRG1, and eight activating receptors KIR2DS3, KIR2DS5, NKp30, NTB-A, CRACC, CD2, CD7 and CD96 were significantly down-regulated (P<0.05) compared with both anginapatients and the controls. There was no statistical difference in receptor expressions between anginapatients and control group. The quantity of natural killer cells was significantly decreased in both infarction and anginapatients compared with normal range (P<0.001). CONCLUSIONS: The significant mRNAs down-regulation of several receptors in myocardial infarction group and reduction in the quantity of natural killer cells in both myocardial infarction and anginapatients showed a quantitative loss and dysfunction of natural killer cells in myocardial infarctionpatients.
Authors: Kristian Thygesen; Joseph S Alpert; Allan S Jaffe; Maarten L Simoons; Bernard R Chaitman; Harvey D White; Kristian Thygesen; Joseph S Alpert; Harvey D White; Allan S Jaffe; Hugo A Katus; Fred S Apple; Bertil Lindahl; David A Morrow; Bernard R Chaitman; Peter M Clemmensen; Per Johanson; Hanoch Hod; Richard Underwood; Jeroen J Bax; Jeroen J Bonow; Fausto Pinto; Raymond J Gibbons; Keith A Fox; Dan Atar; L Kristin Newby; Marcello Galvani; Christian W Hamm; Barry F Uretsky; Ph Gabriel Steg; William Wijns; Jean-Pierre Bassand; Phillippe Menasche; Jan Ravkilde; E Magnus Ohman; Elliott M Antman; Lars C Wallentin; Paul W Armstrong; Maarten L Simoons; James L Januzzi; Markku S Nieminen; Mihai Gheorghiade; Gerasimos Filippatos; Russell V Luepker; Stephen P Fortmann; Wayne D Rosamond; Dan Levy; David Wood; Sidney C Smith; Dayi Hu; Jose-Luis Lopez-Sendon; Rose Marie Robertson; Douglas Weaver; Michal Tendera; Alfred A Bove; Alexander N Parkhomenko; Elena J Vasilieva; Shanti Mendis; Jeroen J Bax; Helmut Baumgartner; Claudio Ceconi; Veronica Dean; Christi Deaton; Robert Fagard; Christian Funck-Brentano; David Hasdai; Arno Hoes; Paulus Kirchhof; Juhani Knuuti; Philippe Kolh; Theresa McDonagh; Cyril Moulin; Bogdan A Popescu; Zeljko Reiner; Udo Sechtem; Per Anton Sirnes; Michal Tendera; Adam Torbicki; Alec Vahanian; Stephan Windecker; Joao Morais; Carlos Aguiar; Wael Almahmeed; David O Arnar; Fabio Barili; Kenneth D Bloch; Ann F Bolger; Hans Erik Botker; Biykem Bozkurt; Raffaele Bugiardini; Christopher Cannon; James de Lemos; Franz R Eberli; Edgardo Escobar; Mark Hlatky; Stefan James; Karl B Kern; David J Moliterno; Christian Mueller; Aleksandar N Neskovic; Burkert Mathias Pieske; Steven P Schulman; Robert F Storey; Kathryn A Taubert; Pascal Vranckx; Daniel R Wagner Journal: J Am Coll Cardiol Date: 2012-09-05 Impact factor: 24.094
Authors: Wei Li; Caroline Lidebjer; Xi-Ming Yuan; Aleksander Szymanowski; Karin Backteman; Jan Ernerudh; Per Leanderson; Lennart Nilsson; Eva Swahn; Lena Jonasson Journal: Atherosclerosis Date: 2008-02-20 Impact factor: 5.162
Authors: Nathalie T Joncker; Nadine C Fernandez; Emmanuel Treiner; Eric Vivier; David H Raulet Journal: J Immunol Date: 2009-04-15 Impact factor: 5.422
Authors: Pascale André; Roberta Castriconi; Marion Espéli; Nicolas Anfossi; Tiffany Juarez; Sophie Hue; Holli Conway; François Romagné; Alessandra Dondero; Marina Nanni; Sophie Caillat-Zucman; David H Raulet; Cristina Bottino; Eric Vivier; Alessandro Moretta; Pascale Paul Journal: Eur J Immunol Date: 2004-04 Impact factor: 5.532