Masuda A, Makino M, Kasajima T
Department of Pathology, Tokyo Women's Medical College, Japan.
Clin Immunol Immunopathol. 1996 Dec;81(3):253-60. doi: 10.1006/clin.1996.0186.
The destruction of the lymphoid follicle (LF) and of the follicular dendritic cell network in the secondary lymphoid organs are major pathological features in murine acquired immunodeficiency syndrome (MAIDS). These pathological changes are associated with functional deficiency of lymphocytes. However, the mechanisms involved have not been established. In MAIDS-susceptible C57BL/6 (B6) mice, the destruction of the LF occurred as early as 2-3 weeks after the infection by LP-BM5 murine leukemia virus (MuLV) and was accompanied by the intrafollicular infiltration of T cells of an unusual phenotype, Thy-1-CD4+. B6 mice, which Thy-1+ T cells had been depleted by the repeated inoculation with monoclonal antibody to Thy-1 antigen, developed LF destruction after infection similar to the control B6 mice. The LP-BM5 MuLV-infected C57BL/6-nu/nu (B6-nu/nu) mice, otherwise resistant to MAIDS induction, also developed these abnormalities following the adoptive transfer of highly purified Thy-1-CD4+ T cells obtained from MAIDS mice. Thus, the production of Thy-1-CD4+ T cells and their infiltration into LF are thought to be involved in triggering the LF destruction. However, the cytolysis of follicular components by activated CD8+ T cells or by LP-BM5 MuLV itself was a less likely mechanism as MAIDS developed in B6 mice depleted of CD8+ T cell. A/J mice, which are resistant to viral infection in the presence of CD8+ T cells, also developed MAIDS and LF destruction after the depletion of CD8+ T cells. Furthermore, no follicular destruction was observed in infected B6-nu/nu mice even though they are highly sensitive to LP-BM5 MuLV.
在鼠类获得性免疫缺陷综合征(MAIDS)中,次级淋巴器官中淋巴滤泡(LF)和滤泡树突状细胞网络的破坏是主要的病理特征。这些病理变化与淋巴细胞的功能缺陷有关。然而,其中涉及的机制尚未明确。在易患MAIDS的C57BL/6(B6)小鼠中,LF的破坏早在感染LP-BM5鼠白血病病毒(MuLV)后2至3周就已发生,并伴有异常表型的T细胞(Thy-1-CD4+)在滤泡内浸润。通过反复接种抗Thy-1抗原单克隆抗体使Thy-1+ T细胞耗竭的B6小鼠,感染后出现了与对照B6小鼠相似的LF破坏。LP-BM5 MuLV感染的C57BL/6-nu/nu(B6-nu/nu)小鼠原本对MAIDS诱导具有抗性,但在接受从MAIDS小鼠获得的高度纯化的Thy-1-CD4+ T细胞的过继转移后,也出现了这些异常。因此,Thy-1-CD4+ T细胞的产生及其向LF的浸润被认为与触发LF破坏有关。然而,由于在CD8+ T细胞耗竭的B6小鼠中也发生了MAIDS,因此激活的CD8+ T细胞或LP-BM5 MuLV本身对滤泡成分的细胞溶解作用不太可能是其机制。在存在CD8+ T细胞时对病毒感染具有抗性的A/J小鼠,在CD8+ T细胞耗竭后也出现了MAIDS和LF破坏。此外,尽管感染的B6-nu/nu小鼠对LP-BM5 MuLV高度敏感,但未观察到滤泡破坏。