Immunologic reactions in amyotrophic lateral sclerosis brain and spinal cord tissue.

Immunologic reactions in amyotrophic lateral sclerosis brain and spinal cord tissue.
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发表时间:
1992-03
期刊:
The American journal of pathology
影响因子:
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通讯作者:
T. Kawamata;H. Akiyama;T. Yamada;P. Mcgeer
T. Kawamata;H. Akiyama;T. Yamada;P. Mcgeer
中科院分区:
其他
文献类型:
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作者:
T. Kawamata;H. Akiyama;T. Yamada;P. Mcgeer

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通过免疫组织化学方法研究了肌萎缩侧索硬化症 (ALS) 患者死后大脑和脊髓中与免疫功能相关的蛋白质的表达。在 ALS 的受影响区域中,反应性小胶质细胞/巨噬细胞表现出高水平的白细胞共同抗原 (LCA)、免疫球蛋白受体 Fc gamma R1、淋巴细胞功能相关分子 1 (LFA-1)、补体受体 CR3 和 CR4、II 类主要组织相容性复合物分子 HLA-DR、HLA-DP 和 HLA-DQ 以及 I 类 HLA-A、B、C 复合物的共同决定簇。这些区域包括初级运动皮层、脑干​​运动核、脊髓前角和整个皮质脊髓束。观察到大量辅助/诱导子 (CD4+) 和细胞毒性/抑制子 (CD8+) 亚型的 T 淋巴细胞沿着毛细血管和小静脉壁边缘化,并延伸到受影响区域的实质。在 ALS 受影响的区域经常检测到补体激活的少突胶质细胞簇以及 C3d 和 C4d 阳性的退化神经突。这些数据提供了 ALS 中免疫效应物变化的证据。它们与该疾病的自身免疫或慢病毒理论一致,但可能仅反映继发性变化。
Expression of proteins associated with immune function was investigated immunohistochemically in postmortem brain and spinal cord of patients with amyotrophic lateral sclerosis (ALS). Reactive microglia/macrophages displaying high levels of leukocyte common antigen (LCA), the immunoglobulin receptor Fc gamma R1, lymphocyte function associated molecule-1 (LFA-1), the complement receptors CR3 and CR4, the class II major histocompatibility complex molecules HLA-DR, HLA-DP and HLA-DQ and common determinants of the class I HLA-A,B,C complex were abundant in affected areas in ALS. These areas included the primary motor cortex, motor nuclei of the brain stem, the anterior horn of the spinal cord, and the full extent of the corticospinal tract. A significant number of T lymphocytes of the helper/inducer (CD4+) and cytotoxic/suppressor (CD8+) subtypes were observed marginating along the walls of capillaries and venules and extending into the parenchyma of affected areas. Clusters of complement activated oligodendroglia as well as degenerating neurites positive for C3d and C4d were frequently detected in ALS-affected areas. These data provide evidence of immune-effector changes in ALS. They are consistent with an autoimmune or slow virus theory of the disorder, but may reflect only secondary changes.