BACKGROUND: Immunoadsorption (IA) is used in patients with inflammatory dilative cardiomyopathy (iDCM) to remove cardiotoxic autoantibodies, and to improve myocardial function. Even if IA is used only once, the level of anti-cardiac antibodies remains low over time. Changes in cell-mediated immunity after IA may contribute to this observation. The aim of this study is to investigate the effect of IA on cell-mediated immunity especially on regulatory and early activated T cells. METHODS: Ten patients (50.1 ± 9.3 years) with chronic iDCM (with signs of myocardial inflammation in biopsies, but without persistence of virus genome), reduced left ventricular ejection fraction (EF < 35%) underwent IA. Blood samples were drawn before and after an IA course of 5 days, and 1, 3, and 6 months after IA. Leukocyte subpopulations were quantified by FACS analysis. RESULTS: Left ventricular systolic function improved on average at 6 months from 25.6 ± 4.9 to 37.3 ± 10.1% (p < 0.05). The left ventricular end-diastolic diameter was reduced after 6 months (63.3 ± 3.1 vs. 57.1 ± 4.1 mm; p < 0.05). IA therapy led to an increase of regulatory T cells (CD4(+), CD25(+) and CD127(low)) over time (up to 6 months). This was associated with a decrease of activated T cells (CD4(+)/CD69(+) and CD8(+)/CD69(+) cells) and CD28(+) T cells (co-stimulatory cells), which was detectable for at least 6 months after IA. CONCLUSION: It is suggested that changes in cell-mediated immunity contribute to the beneficial effect of IA on myocardial function, and on maintenance of reduced blood levels of cardiotoxic autoantibodies.
BACKGROUND: Immunoadsorption (IA) is used in patients with inflammatory dilative cardiomyopathy (iDCM) to remove cardiotoxic autoantibodies, and to improve myocardial function. Even if IA is used only once, the level of anti-cardiac antibodies remains low over time. Changes in cell-mediated immunity after IA may contribute to this observation. The aim of this study is to investigate the effect of IA on cell-mediated immunity especially on regulatory and early activated T cells. METHODS: Ten patients (50.1 ± 9.3 years) with chronic iDCM (with signs of myocardial inflammation in biopsies, but without persistence of virus genome), reduced left ventricular ejection fraction (EF < 35%) underwent IA. Blood samples were drawn before and after an IA course of 5 days, and 1, 3, and 6 months after IA. Leukocyte subpopulations were quantified by FACS analysis. RESULTS:Left ventricular systolic function improved on average at 6 months from 25.6 ± 4.9 to 37.3 ± 10.1% (p < 0.05). The left ventricular end-diastolic diameter was reduced after 6 months (63.3 ± 3.1 vs. 57.1 ± 4.1 mm; p < 0.05). IA therapy led to an increase of regulatory T cells (CD4(+), CD25(+) and CD127(low)) over time (up to 6 months). This was associated with a decrease of activated T cells (CD4(+)/CD69(+) and CD8(+)/CD69(+) cells) and CD28(+) T cells (co-stimulatory cells), which was detectable for at least 6 months after IA. CONCLUSION: It is suggested that changes in cell-mediated immunity contribute to the beneficial effect of IA on myocardial function, and on maintenance of reduced blood levels of cardiotoxic autoantibodies.
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