论文部分内容阅读
AIM:To study the individual effects of glucocorticoid (GC) therapy on the state ofimmune activation in patient serum.METHODS:We developed a novel assay in which the effect of corticosteroid-treated patient serum on healthy donor peripheral blood mononuclear cells (target cells) was studied,with a panel of markers for effector [interferon (IFN)γ and interleukin (IL)-5] and regulatory T cells (FOXP3 and glucocorticoid-induced tumor necrosis factor receptor,GITR).The study group comprised 19 children with inflammatory bowel disease.The individual effect of patient serum on target cells was analyzed prior to GC therapy and 2 wk later.RESULTS:The effect of GC therapy mediated by patient serum was seen as a decrease in the target cells expression of regulatory T-cell-related markers GITR (median suppression 24%,range of suppression 1%-63%,in 2 cases increase of 6% and 77%,P < 0.01 for mitogen-activated target cells) and FOXP3 (median suppression 33%,range of suppression 0%-79%,in one case an increase of 173%,P < 0.05 for resting cells),and secretion of IFNγ [from a mean of 87 700 pg/mL (SD 33 900 pg/mL) to 60 900 pg/mL (SD 44 200 pg/mL) in mitogen-activated target cells,13 of the cases showed a decrease,P < 0.01].The total or weight-related prednisolone dose did not correlate with the patient-seruminduced changes in the target cell markers.CONCLUSION:GC response could be monitored at an individual level by studying the effect of patient serum on signaling pathways of target immune cells.
AIM: To study the individual effects of glucocorticoid (GC) therapy on the state ofimmune activation in patient serum. METHODS: We developed a novel assay in which the effect of corticosteroid-treated patient serum on healthy donor peripheral blood mononuclear cells (target cells) was studied with a panel of markers for effector [interferon (IFN) γ and interleukin (IL) -5] and regulatory T cells (FOXP3 and glucocorticoid-induced tumor necrosis factor receptor, GITR) bowel disease. The individual effect of patient serum on target cells was analyzed prior to GC therapy and 2 wk later .RESULTS: The effect of GC therapy mediated by patient serum was as as decrease in the target cells expression of regulatory T-cell- Related markers GITR (median suppression 24%, range of suppression 1% -63%, in 2 cases increase of 6% and 77%, P <0.01 for mitogen-activated target cells) and FOXP3 (median suppression 33%, range of suppression 0% -79%, in one case a n increase of 173%, P <0.05 for resting cells, and secretion of IFNγ to 60 900 pg / mL (SD 44 200 pg / mL) in mitogen-activated target cells, 13 of the cases showed a decrease, P <0.01]. The total or weight-related prednisolone dose did not correlate with the patient-serum induced changes in the target cell markers. CONCLUSION: GC response could monitored at an individual level by studying the effect of patient serum on signaling pathways of target immune cells.