Eosinophilia myalgia syndrome: I. Immunocytochemical evidence for a T-cell-mediated immune effector response
Autor: | Andrew G. Engel, Alison M. Emslie-Smith, Joseph R. Duffy, Carolyn A. Bowles |
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Rok vydání: | 1991 |
Předmět: |
Adult
Male T-Lymphocytes T cell CD1 Fluorescent Antibody Technique Complement Membrane Attack Complex Biology Major histocompatibility complex Natural killer cell Major Histocompatibility Complex Eosinophilia–myalgia syndrome Immune system Muscular Diseases Antigens CD Eosinophilia medicine Humans Fascia Aged Immunity Cellular Macrophages Muscles Syndrome Middle Aged Natural killer T cell medicine.disease Immunohistochemistry medicine.anatomical_structure Neurology Immunology biology.protein Female Neurology (clinical) CD8 |
Zdroj: | Annals of Neurology. 29:524-528 |
ISSN: | 1531-8249 0364-5134 |
DOI: | 10.1002/ana.410290512 |
Popis: | Specimens of muscle and fascia from 13 patients fulfilling the Centers for Disease Control criteria for the eosinophilia myalgia syndrome (EMS) were studied by quantitative immunocytochemical analysis. The immunolocalization of CD3, CD4, CD8, CD22, and CD56 markers, the gamma delta T-cell receptor, major histocompatibility complex (MHC) class I complex and class II antigens, and complement membrane attack complex (MAC) were examined. The distribution and relative proportions of T cells and T-cell subsets, B cells, macrophages, and eosinophils were determined at perivascular, perimysial, endomysial, and fascial sites of accumulation. At all sites, T cells were predominant, CD8+ cells outnumbered CD4+ cells 6- to 20-fold, and between 60 and 80% of T cells were activated. B cells and eosinophils each accounted for less than 3% of inflammatory cells. Very few cells expressed either the gamma delta T-cell receptor or natural killer cell markers. As in dermatomyositis (DM), MHC class I antigen complex expression was increased on many structurally normal muscle fibers, but in contrast to DM, microvascular MAC deposits were not a feature of EMS. The findings implicate a cellular immune response directed against a connective tissue component in EMS. |
Databáze: | OpenAIRE |
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