The Journal of rheumatology · 2004
MHC Class I overexpression on muscles in early juvenile dermatomyositis.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Li Charles K C, Varsani Hemlata, Holton Janice L, Gao Bin, Woo Patricia, Wedderburn Lucy R, Juvenile Dermatomyositis Research Group (UK and Ireland)
Аннотация
OBJECTIVE: To assess muscle expression of MHC Class I complexes (heavy chain and beta2-microglobulin) and to analyze the composition of infiltrating mononuclear cells, specifically cells that bear receptors for class I MHC molecules, in the muscles of children with early juvenile dermatomyositis (JDM).
METHODS: Light microscopic and immunohistochemical analysis of muscle biopsies from 10 patients with JDM and 3 controls. The mean duration from initial weakness was 2.8 months. At the time of biopsy, 9 patients had not received steroid treatment or immunomodulatory drugs.
RESULTS: MHC Class I over-expression was evident on muscle fibers in all 10 JDM samples, even in a biopsy reported as normal by conventional histology. MHC class I heavy chain and beta2-microglobulin were over-expressed in an identical distribution. Variable infiltration of T cells and macrophages was seen in the JDM biopsies, with minimal lymphocytic and monocytic infiltration in 4 cases, and none in one. Only very occasional natural killer lymphocytes were identified. Neuronal cell adhesion molecule (NCAM, CD56) staining of regenerating muscle fibers was seen in all samples and these cells were confirmed as being of muscle origin by co-staining for dystrophin.
CONCLUSION: MHC Class I over-expression is an early event in JDM, and may occur in the absence of lymphocytic infiltration and muscle damage. Immunostaining for MHC Class I could be used routinely in the assessment of muscle histology in juvenile dermatomyositis.
METHODS: Light microscopic and immunohistochemical analysis of muscle biopsies from 10 patients with JDM and 3 controls. The mean duration from initial weakness was 2.8 months. At the time of biopsy, 9 patients had not received steroid treatment or immunomodulatory drugs.
RESULTS: MHC Class I over-expression was evident on muscle fibers in all 10 JDM samples, even in a biopsy reported as normal by conventional histology. MHC class I heavy chain and beta2-microglobulin were over-expressed in an identical distribution. Variable infiltration of T cells and macrophages was seen in the JDM biopsies, with minimal lymphocytic and monocytic infiltration in 4 cases, and none in one. Only very occasional natural killer lymphocytes were identified. Neuronal cell adhesion molecule (NCAM, CD56) staining of regenerating muscle fibers was seen in all samples and these cells were confirmed as being of muscle origin by co-staining for dystrophin.
CONCLUSION: MHC Class I over-expression is an early event in JDM, and may occur in the absence of lymphocytic infiltration and muscle damage. Immunostaining for MHC Class I could be used routinely in the assessment of muscle histology in juvenile dermatomyositis.