van Gelder M, Kinwel-Bohré E P, Mulder A H, van Bekkum D W
Introgene, Rijswijk, The Netherlands.
Cell Immunol. 1996 Feb 25;168(1):39-48. doi: 10.1006/cimm.1996.0047.
To determine the feasibility of treatment with allogeneic bone marrow for experimental autoimmune encephalomyelitis, we investigated the susceptibility to experimental autoimmune encephalomyelitis of bone marrow chimeras using BUF, (WAG X BUF)F1 (high responder), and WAG (low responder) rats. In contrast to previous studies in which other rat strains were used, the response was largely determined by the genotype of the grafted bone marrow, but the influence of a non-bone marrow-associated factor was evident. The latter factor was identified as a low corticosterone response in BUF rats and a high corticosterone response in WAG rats. After adrenalectomy, a significant proportion of WAG rats developed clinical experimental autoimmune encephalomyelitis. The bone marrow-associated factor of resistance appeared to be the activity of cyclophosphamide-sensitive suppressor cells. The latter cells were found to interfere with the formation of inflammatory foci in the central nervous system, while corticosterone primarily prevents the clinical expression of lesions.
为了确定同种异体骨髓治疗实验性自身免疫性脑脊髓炎的可行性,我们使用BUF、(WAG×BUF)F1(高反应者)和WAG(低反应者)大鼠研究了骨髓嵌合体对实验性自身免疫性脑脊髓炎的易感性。与之前使用其他大鼠品系的研究不同,反应很大程度上由移植骨髓的基因型决定,但非骨髓相关因素的影响也很明显。后一种因素被确定为BUF大鼠的低皮质酮反应和WAG大鼠的高皮质酮反应。肾上腺切除术后,相当比例的WAG大鼠发生了临床实验性自身免疫性脑脊髓炎。骨髓相关的抗性因素似乎是环磷酰胺敏感抑制细胞的活性。发现后一种细胞会干扰中枢神经系统炎症病灶的形成,而皮质酮主要阻止病变的临床表现。