Aoki I, Aoki A, Otani M, Miyagi Y, Misugi K, Ishii N, Hagiwara E, Tani K, Okubo T, Ishigatsubo Y
Department of Pathology, Yokohama City University School of Medicine, Japan.
Clin Immunol Immunopathol. 1992 Apr;63(1):34-8. doi: 10.1016/0090-1229(92)90090-b.
A graft-versus-host reaction (GVHR) was induced in (B10 x DBA/2)F1 (BDF1) and (BALB/c x A)F1 (CAF1) murine recipients by injection of their parental or B10.D2-derived spleen cells. The incidences of glomerulonephritis and autoantibody production were then correlated. All of the BDF1 mice that received DBA/2 spleen cells (termed DBA/2----BDF1) and 33% of the CAF1 mice that received BALB/c spleen cells (BALB/c----CAF1) developed glomerulonephritis. However, in other combinations (B10.D2----BDF1, A/J----CAF1) no significant glomerular lesions were observed. An analysis of antibodies by ELISA revealed that the groups with renal disease showed a significant polyclonal elevation of IgG class antibodies, including autoantibodies (anti-DNA, anti-MRBC, and NTA) and a conventional antibody (anti-TNP-KLH). No significant IgG class antibody production was observed in the groups that did not develop glomerulonephritis. Thus, it was suggested that an IgM to IgG class switch is important in the development of glomerulonephritis in GVHR. Other factors also appear to be involved. Only 33% of BALB/c----CAF1 developed glomerulonephritis, even though a level of IgG class antibody production was comparable to that observed in DBA/2----BDF1 in which 100% showed severe glomerulonephritis.
通过注射亲代或B10.D2来源的脾细胞，在（B10×DBA/2）F1（BDF1）和（BALB/c×A）F1（CAF1）小鼠受体中诱导移植物抗宿主反应（GVHR）。然后将肾小球肾炎的发病率与自身抗体产生进行关联分析。所有接受DBA/2脾细胞的BDF1小鼠（称为DBA/2→BDF1）以及33%接受BALB/c脾细胞的CAF1小鼠（BALB/c→CAF1）发生了肾小球肾炎。然而，在其他组合（B10.D2→BDF1，A/J→CAF1）中未观察到明显的肾小球病变。通过ELISA对抗体进行分析发现，患有肾脏疾病的组中IgG类抗体出现显著的多克隆升高，包括自身抗体（抗DNA、抗MRBC和NTA）以及一种传统抗体（抗TNP-KLH）。在未发生肾小球肾炎的组中未观察到明显的IgG类抗体产生。因此，提示在GVHR中，IgM向IgG类的转换在肾小球肾炎的发生中起重要作用。其他因素似乎也参与其中。尽管BALB/c→CAF1组中IgG类抗体产生水平与DBA/2→BDF1组相当，而DBA/2→BDF1组中100%表现为严重的肾小球肾炎，但BALB/c→CAF1组中只有33%发生了肾小球肾炎。
