Objectives: To determine whether muscle weakness is correlated with inflammation, expression of interleukin 1α (IL1α) and major histocompatibility complex (MHC) class I and II antigens on muscle fibres.
Methods: Biopsy specimens from clinically symptomatic (proximal muscles) and asymptomatic (all distal but two proximal) muscles in eight patients with polymyositis, three patients with dermatomyositis and six healthy controls were analysed by immunohistochemistry for the presence of T cells and macrophages, and expression of IL1α and of MHC class I and II antigens. Results were evaluated by conventional light microscopy and by computerised image analysis.
Results: Inflammatory infiltrates with T cells and macrophages were observed to an equal degree in both symptomatic and asymptomatic muscle. The numbers of capillaries with IL1α expression were significantly higher (p<0.05) in the symptomatic and asymptomatic muscles of patients than in controls. The total IL1α expression per tissue section assessed by computerised image analysis was significantly higher in symptomatic muscles but not in asymptomatic muscles compared with that in controls. Neither the number of IL1α-positive capillaries nor the total IL1α expression differed significantly between symptomatic and asymptomatic muscles. Expression of MHC class I and II antigens on muscle fibres was detected in both symptomatic and asymptomatic muscles but rarely in healthy controls.
Conclusions: Presence of inflammatory infiltrates, T cells and macrophages, and expression of MHC class I and II antigens and of IL1α on muscle fibres were independent of clinical symptoms, and were present to an equal degree in both proximal and distal muscles. Thus, other factors seem to determine the development of clinical symptoms. One such factor could be variations in physical demands.
- EMG, electromyography
- HLA, human leucocyte antigen
- MHC, major histocompatibility complex
- MRI, magnetic resonance imaging
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Published Online First 10 July 2006
Funding: This study was supported by grants from the Swedish Rheumatism Association, King Gustaf Vth 80-year Foundation, the Swedish Research Council 2002-74X-14045-02A, Professor Nanna Svartz Foundation, Magnus Bergvalls Foundation, Börje Dahlin Foundation, Stiftelsen Clas Groschinskys Minnesfond, Karolinska Institutet Foundation and the Vardal Foundation.
Competing interests: None.