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ANTIGEN PRESENTATION IS INHIBITED IN VIVO BY BETAMETHASONE

机译:倍他米松可抑制体内抗原的表达

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Aim of the present study was to assess whether betamethasone, a synthetic glucocorticoid used as immunosuppressant, could modify in vivo the antigen presentation by antigen presenting cells (APC). Interleukin-2 (IL-2) production by a T cell hybridoma specific for the hen egg white lysozyme (HEL) cultured in the presence of HEL and APC from treated or control mice was utilized as read out. Betamethasone induced a dose-dependent inhibition of antigen presentation. Fifty percent maximal response was observed with 1152 (95% confidence interval: 948-1419) resident peritoneal macrophages from untreated animals, and 5843 (4700-7445), 21,235 (12,857-43,705), 28,313 (20,847-40,955) macrophages from mice injected for 3 days with betamethasone 10, 25, and 50 mg/kg respectively. Similar findings were obtained with spleen cells. When given for 3 days al 25 mg/kg, betamethasone reduced the number of cells recovered from the peritoneum by approximately half and from the spleen by one order of magnitude. One day vs. 3 days treatment resulted in similar recovery of cells but lower inhibition of APC function. In the experimental conditions utilized, no carryover of betamethasone with APC could be demonstrated and no reversal of inhibition was observed by increasing the antigen concentration. The data here presented demonstrate that short curses of high dose betamethasone specifically impair antigen presentation. Thus, this mechanism appears to be involved in the immunosuppressant activity of betamethasone. [References: 10]
机译:本研究的目的是评估倍他米松(一种用作免疫抑制剂的合成糖皮质激素)是否可以在体内改变抗原呈递细胞(APC)的抗原呈递。读出的是利用在HEL和APC存在下培养的对鸡蛋清溶菌酶(HEL)特异的T细胞杂交瘤产生的白细胞介素2(IL-2)。倍他米松诱导了抗原呈递的剂量依赖性抑制。观察到来自未经治疗的动物的1152(常置信区间:948-1419)常驻腹膜巨噬细胞以及分别来自注射的小鼠的5843(4700-7445),21,235(12,857-43,705),28,313(20,847-40,955)巨噬细胞的最大应答率为50%分别用倍他米松10、25和50 mg / kg服用3天。脾细胞也有类似的发现。当以25 mg / kg的剂量给予3天时,倍他米松将从腹膜中回收的细胞数量减少了一半,从脾脏中回收的细胞数量减少了一个数量级。一日与三天的治疗导致相似的细胞恢复,但对APC功能的抑制作用较低。在所利用的实验条件下,没有证明倍他米松与APC残留,并且通过增加抗原浓度没有观察到抑制作用的逆转。此处提供的数据表明,大剂量倍他米松的短时间治愈会特别损害抗原呈递。因此,该机制似乎与倍他米松的免疫抑制活性有关。 [参考:10]

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