Revelli S, Dávila H, Moreno H, Bottasso O
Immunology Division, Faculty of Medical Sciences, Universidad Nacional de Rosario, Argentina.
J Rheumatol. 1992 Apr;19(4):513-6.
Chronically Trypanosoma cruzi infected "I" rats and syngeneic naive recipients, transferred with a T cell enriched spleen cell population from infected donors, develop an attenuated arthritis when challenged with complete Freund's adjuvant. We report that cyclophosphamide, 40 mg/kg body weight, given 48 h before induction, was able to reestablish or exacerbate adjuvant arthritis in infected and control rats, respectively. Although the T cell enriched spleen cells from infected donors continued to down regulate adjuvant arthritis in syngeneic recipients given cyclophosphamide 48 h before cell transfer, treatment of infected donors with cyclophosphamide, 48 h before cell collection, prevented these cells from exerting such effect when transferred to healthy recipients receiving no cyclophosphamide. It is suggested that cyclophosphamide may primarily affect a suppressor cell population, present in the infected host, with regulatory activity on adjuvant arthritis.
长期感染克氏锥虫的“I”系大鼠以及同基因未感染的受体大鼠,接受来自感染供体的富含T细胞的脾细胞群体移植后,在用完全弗氏佐剂攻击时会发生轻度关节炎。我们报告,在诱导前48小时给予40mg/kg体重的环磷酰胺,能够分别在感染大鼠和对照大鼠中重建或加重佐剂性关节炎。尽管来自感染供体的富含T细胞的脾细胞在细胞移植前48小时给予环磷酰胺的同基因受体中继续下调佐剂性关节炎,但在细胞收集前48小时用环磷酰胺处理感染供体,当将这些细胞转移到未接受环磷酰胺的健康受体时,会阻止这些细胞发挥这种作用。提示环磷酰胺可能主要影响感染宿主中存在的具有调节佐剂性关节炎活性的抑制细胞群体。