Ito S, Ueno M, Nishi S, Arakawa M, Ikarashi Y, Saitoh T, Fujiwara M
Department of Medicine (II), Niigata University School of Medicine, Japan.
Autoimmunity. 1992;12(2):79-87. doi: 10.3109/08916939209150313.
Renal lesions at the chronic phase of MHC class-II-disparate graft-versus-host reaction (GVHR) were examined. To induce GVHR, C57BL/6 (B6) spleen cells were injected twice into either (B6 x bm12)F1 (class-II-disparate), (B6 x bm1)F1 (class-I-disparate) or (bm1 x bm12)F1 mice (class-I + II-disparate). For comparison, (C57BL/10 x DBA/2)F1 (BDF1) mice injected with DBA/2 spleen cells were also used. (B6 x bm12)F1 and BDF1 recipients showed marked elevation of anti-DNA antibodies, circulating immune complexes (CIC) and the number of immunoglobulin producing cells (IgPC). At 20 weeks after cell injection, severe immune complex glomerulonephritis (ICGN) was observed in (B6 x bm12)F1 recipients, but was far less severe in (bm1 x bm12)F1 recipients and was not observed in (B6 x bm1)F1 recipients. ICGN was also observed in BDF1 recipients at 12 weeks after cell injection. By immunofluorescent microscopy, IC deposition was detected along the capillary loops and also in the mesangial area in (B6 x bm12)F1 recipients, while BDF1 recipients showed only a capillary pattern. By light microscopy, the renal lesion of (B6 x bm12)F1 recipients appeared similar to those of BDF1 recipients. Histologically, (B6 x bm12)F1 recipients serve as a good model for lupus glomerulonephritis induced by class-II-disparate GVHR.
对MHC II类不相合移植物抗宿主反应（GVHR）慢性期的肾脏病变进行了检查。为诱导GVHR，将C57BL/6（B6）脾细胞分两次注射到（B6×bm12）F1（II类不相合）、（B6×bm1）F1（I类不相合）或（bm1×bm12）F1小鼠（I类+II类不相合）体内。作为对照，还使用了注射DBA/2脾细胞的（C57BL/10×DBA/2）F1（BDF1）小鼠。（B6×bm12）F1和BDF1受体小鼠的抗DNA抗体、循环免疫复合物（CIC）以及免疫球蛋白产生细胞（IgPC）数量显著升高。细胞注射后20周，在（B6×bm12）F1受体小鼠中观察到严重的免疫复合物性肾小球肾炎（ICGN），但在（bm1×bm12）F1受体小鼠中严重程度要低得多，而在（B6×bm1）F1受体小鼠中未观察到。在细胞注射后12周，BDF1受体小鼠中也观察到了ICGN。通过免疫荧光显微镜检查，在（B6×bm12）F1受体小鼠的毛细血管袢及系膜区均检测到IC沉积，而BDF1受体小鼠仅表现为毛细血管模式。通过光学显微镜检查，（B6×bm12）F1受体小鼠的肾脏病变与BDF1受体小鼠相似。组织学上，（B
