Elsevier

Human Pathology

Volume 20, Issue 3, March 1989, Pages 224-231
Human Pathology

Original contribution
Major histocompatibility complex class I antigen expression, immunolocalization of interferon subtypes, and T cell-mediated cytotoxicity in myopathies

https://doi.org/10.1016/0046-8177(89)90128-7Get rights and content

Abstract

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, myrial muscle fibers expressed MHC-I, but none were invadedy by CD8+ cells. In all disease, 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.

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  • Cited by (0)

    Supported in part by NIH grant no. NS 6277 and a Research Center grant from the Muscular Dystrophy Association. During this study, A. M. E. held and MDA Clinical Fellowship and a travel award from the Wellcome Trust and K. A. received support from the Mogg Fund.

    Present address: National Institute of Neuroscience, NCNP, Tokyo, Japan.

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