Joseph L J, Iwasaki T, Malek T R, Shearer G M
J Immunol. 1985 Sep;135(3):1846-50.
Mice of the (C57BL/10 X B10.A)F1 combination were given a single i.v. inoculation of 3 to 4 X 10(7) B10.A spleen cells, which induces a graft-vs-host (GVH)-associated immune deficiency in F1 mice. Between 1 and 4 wk later, spleen cells from the F1 mice were tested for the expression of IL 2 receptors by flow microfluorometry, using the 7D4 rat monoclonal antibody directed against an epitope murine IL 2 receptor. A reduction in intensity of spleen cell staining with 7D4 was detected as early as 8 days after parental cell inoculation, and no IL 2 receptors were detected by 28 days after initiation of GVH. Furthermore, the loss of IL 2 receptors was correlated with abrogation of proliferative responses to concanavalin A and lipopolysaccharide, of IL 2 production, and of cytotoxic T lymphocyte responses. These observations may be relevant for our understanding of GVH reactions, of immune disorders associated with GVH, and possibly of primary and acquired immunodeficiencies in general.
给(C57BL/10×B10.A)F1组合的小鼠静脉内单次接种3至4×10⁷个B10.A脾细胞,这会在F1小鼠中诱导与移植物抗宿主(GVH)相关的免疫缺陷。1至4周后,使用针对鼠IL-2受体表位的7D4大鼠单克隆抗体,通过流式微荧光法检测F1小鼠脾细胞中IL-2受体的表达。早在亲代细胞接种后8天就检测到用7D4染色的脾细胞强度降低,并且在GVH开始后28天未检测到IL-2受体。此外,IL-2受体的丧失与对伴刀豆球蛋白A和脂多糖的增殖反应、IL-2产生以及细胞毒性T淋巴细胞反应的消除相关。这些观察结果可能与我们对GVH反应、与GVH相关的免疫紊乱以及可能一般的原发性和获得性免疫缺陷的理解有关。