Morrissey P J, Charrier K
Immunex Research and Development Corporation, Seattle, WA 98101, USA.
Res Immunol. 1994 Jun;145(5):357-62. doi: 10.1016/s0923-2494(94)80200-9.
SCID mice injected with coisogenic CD4+/CD45RBhi lymph node T cells from normal donors develop a wasting disease that is due to hyperplasia of the intestinal epithelium. SCID mice injected with purified lymph node CD4+ T cells or CD4+/CD45RBlo T cells do not develop the disease. In addition, mixture of the CD4+/CD45RBlo T cells with equal numbers of CD4+/CD45RBhi T cells inhibits the development of disease. SCID mice that were reconstituted with CD45RBhi T cells with active disease were treated with oral antibiotics and this ameliorated the symptoms, suggesting a role of the gut bacterial flora in the development of disease. Attempts were made to accelerate or inhibit disease by chronically administering cytokines to the mice. Neither IL2 nor IL4 were effective in altering the course of disease development when given in doses known to be effective in other in vivo models. Thus, the regulation of the reactivity seen in these SCID mice may involve as yet unappreciated mechanisms.
给SCID小鼠注射来自正常供体的同基因CD4⁺/CD45RBhi淋巴结T细胞，会引发一种消耗性疾病，该疾病是由肠道上皮细胞增生所致。给SCID小鼠注射纯化的淋巴结CD4⁺ T细胞或CD4⁺/CD45RBlo T细胞则不会引发这种疾病。此外，将CD4⁺/CD45RBlo T细胞与等量的CD4⁺/CD45RBhi T细胞混合，可抑制疾病的发展。对患有活动性疾病的用CD45RBhi T细胞重建的SCID小鼠给予口服抗生素治疗，症状得到改善，这表明肠道细菌菌群在疾病发展中起作用。尝试通过长期给小鼠施用细胞因子来加速或抑制疾病。当以已知在其他体内模型中有效的剂量给予时，IL2和IL4均不能有效改变疾病发展进程。因此，这些SCID小鼠中所见反应性的调节可能涉及尚未被认识的机制。
