Aoki A, Ishigatsubo Y, Hagiwara E, Shirai A, Igarashi T, Tani K, Maruta A, Otani M, Aoki I, Misugi K
First Department of Internal Medicine, Yokohama City University School of Medicine, Japan.
Clin Immunol Immunopathol. 1993 Mar;66(3):254-9. doi: 10.1006/clin.1993.1033.
Primary chronic graft-versus-host reaction (GVHR) was induced in (C57BL/10 x DBA/2)F1 (BDF1) mice via the transfer of parental DBA/2 derived lymphocytes. A significant increase in the absolute number of IgM- and IgG-secreting cells was found in recipient BDF1 mice at 3 weeks post-transfer. The increase included B cells reactive with both self- and non-self-antigens, without being skewed toward the production of autoantibodies. Later in the disease process (approximately 6-8 weeks post-transfer), we detected an increased number of B cells that secreted antibodies reactive with a select subset of autoantigens in about 30% of BDF1 recipients (3 of 9 mice). These findings suggest that not only antigen-specific stimulation, which was detected in a late stage, but also initial polyclonal activation may account for chronic GVHR.
通过转移亲本DBA/2来源的淋巴细胞，在（C57BL/10×DBA/2）F1（BDF1）小鼠中诱导出原发性慢性移植物抗宿主反应（GVHR）。在转移后3周，受体BDF1小鼠中分泌IgM和IgG的细胞绝对数量显著增加。这种增加包括与自身和非自身抗原均反应的B细胞，且未偏向自身抗体的产生。在疾病过程后期（转移后约6 - 8周），我们在约30%的BDF1受体（9只小鼠中的3只）中检测到分泌与特定自身抗原亚群反应抗体的B细胞数量增加。这些发现表明，不仅在晚期检测到的抗原特异性刺激，而且初始的多克隆激活都可能是慢性GVHR的原因。
