Author/Authors :
Mahmoudi، Mohammad Jafar نويسنده Division of Cardiology, Department of Internal Medicine, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran Mahmoudi, Mohammad Jafar , Hedayat، Mona نويسنده Division of Cardiology, Department of Internal Medicine, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran AND Research Center for Immunodeficiencies, Pediatrics Center of Excellence, Childrens Medical Center, Tehran University of Medical Sciences, Tehran, Iran Hedayat, Mona , Rezaei، Nima نويسنده , , Saboor-Yaraghi، Ali Akbar نويسنده Department of Nutrition and Biochemistry, School of Public Health, Tehran University of Medical Sciences,Tehran, Iran , , Mahmoudi، Maryam نويسنده Medical Student. Rafsanjan University of Medical Sciences, Rafsanjan, Iran. ,
Abstract :
The CD30 antigen seems to play a costimulatory role in maintaining the physiological balance between T-helper (Th)1/Th2 immune responses. In this study, plasma and in vitro soluble CD30 (sCD30) secretion was investigated in patients with coronary artery disease (CAD) as a plausible marker of dysregulated immune response.
Twenty one patients with angiographically confirmed CAD and 31 healthy controls took part in this study. The levels of the activation marker sCD30 were determined in plasma and phytohaemagglutinin (PHA)-stimulated and unstimulated peripheral blood mononuclear cell cultures by ELISA.
Plasma sCD30 levels did not differ significantly between the patients and controls. However, spontaneous sCD30 secretion was significantly lower in patients with CAD compared to controls (p < 0.001). The soluble CD30 levels were significantly increased in the supernatant of PHA-stimulated PBMCs compared to unstimulated cultures in both groups of patients and controls (p < 0.001). PHA-stimulated sCD30 secretion was found to be lower in patients compared to controls; however, the difference was not statistically significant.
Plasma sCD30 levels were not statistically different in patients with chronic stable CAD, a well-known Th1-mediated disease, compared to controls; whereas decreased spontaneous and PHA-stimulated sCD30 secretion in patients with CAD might indicate the progressive shift towards a Th1 immune response.
