MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-I ANTIGEN EXPRESSION, IMMUNOLOCALIZATION OF INTERFERON SUBTYPES, AND T-CELL-MEDIATED CYTO-TOXICITY IN MYOPATHIES
MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-I ANTIGEN EXPRESSION, IMMUNOLOCALIZATION OF INTERFERON SUBTYPES, AND T-CELL-MEDIATED CYTO-TOXICITY IN MYOPATHIES
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DOI：
10.1016/0046-8177(89)90128-7
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发表时间：
1989-03-01
期刊：
影响因子：
3.3
通讯作者：
ENGEL, AG
中科院分区：
文献类型：
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作者：
EMSLIESMITH, AM;ARAHATA, K;ENGEL, AG
靶细胞上主要组织相容性复合物 I 类 (MHC-I) 的表达是抗原特异性 T 细胞介导的细胞毒性 (TCMC) 的先决条件。 MHC-I 表达增强归因于炎症细胞释放的干扰素 (IFN)。在之前的研究中，我们在多发性肌炎 (PM) 和包涵体肌炎 (IBM) 中发现了 TCMC（细胞毒性 T 细胞侵入非坏死肌纤维）的证据。我们偶尔在杜氏营养不良 (DD) 中发现 TCMC 的证据，但在皮肌炎 (DM) 中却没有发现。本研究探讨了这些疾病和正常对照中 TCMC、MHC-I 表达和 IFN 免疫反应性之间的关系。在对照组中，MHC-I 的反应性仅限于血管。在所有疾病中，再生纤维都表达 MHC-I。在IBM、PM和DD中，所有被CD8+细胞侵入的非坏死肌纤维和一些邻近纤维表达MHC-I。在 DM 中，无数肌纤维表达 MHC-I，但没有一个肌纤维被 CD8+ 细胞侵袭。在所有疾病中，只有少数单核细胞且没有肌纤维表面对干扰素有免疫反应。我们的结论是，肌纤维上的 MHC-I 表达对于肌病的 TCMC 是必要的，但还不够； DM 中 MHC-I 表达增加的生物学意义仍不清楚；目前可用且适当控制的免疫细胞化学方法显示肌纤维上 MHC-I 表达增加与单核细胞局部 IFN 合成之间没有关系。
Major histocompatibility complex class I (MHC-I) expression on target cells is a prerequisite for antigen-specific T cell-mediated cytotoxicity (TCMC). Enhanced MHC-I expression has been attributed to interferons (IFNs) released from inflammatory cells. In previous studies, we found evidence of TCMC (invasion of non-necrotic muscle fibers by cytotoxic T cells) in polymyositis (PM) and in inclusion body myositis (IBM). We occasionally found evidence of TCMC in Duchenne dystrophy (DD) but not in dermatomyositis (DM). This study examines the relationships between TCMC, MHC-I expression, and IFN immunoreactivity in these diseases and normal controls. In controls, reactivity for MHC-I was confined to blood vessels. In all diseases, regenerating fibers expressed MHC-I. In IBM, PM and DD, all nonnecrotic muscle fibers invaded by CD8+ cells and some adjacent fibers expressed MHC-I. In DM, myriad muscle fibers expressed MHC-I, but none were invaded by CD8+ cells. In all diseases, only a few mononuclear cells and no muscle fiber surfaces were immunoreactive for IFNs. We conclude that MHC-I expression on muscle fibers is necessary but not sufficient for TCMC in myopathy; that the biological significance of increased MHC-I expression in DM remains undefined; and that currently available and appropriately controlled immunocytochemical methods show no relationship between increased MHC-I expression on muscle fibers and local IFN synthesis by mononuclear cells.