Signs of inflammation in both symptomatic and asymptomatic muscles from patients with polymyositis and dermatomyositis.
OBJECTIVE
To determine whether muscle weakness is correlated with inflammation, expression of interleukin 1alpha (IL1alpha) 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 IL1alpha 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 IL1alpha expression were significantly higher (p<0.05) in the symptomatic and asymptomatic muscles of patients than in controls. The total IL1alpha 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 IL1alpha-positive capillaries nor the total IL1alpha 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 IL1alpha 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.
Dorph
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C
Rheumatology Unit, Department of Medicine, Karolinska University Hospital, Karolinska Institutet, Solna, Sweden. Christina.Dorph@karolinska.se
Englund
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P
Nennesmo
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Lundberg
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IE
D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D001706:Biopsy; D017252:CD3 Complex / Q000378:metabolism; D003882:Dermatomyositis / Q000276:immunology / Q000473:pathology; D005260:Female; D006684:HLA-DR Antigens / Q000378:metabolism; D015395:Histocompatibility Antigens Class I / Q000378:metabolism; D006801:Humans; D053582:Interleukin-1alpha / Q000378:metabolism; D008264:Macrophages / Q000473:pathology; D008297:Male; D008875:Middle Aged; D018485:Muscle Fibers, Skeletal / Q000276:immunology / Q000473:pathology; D018482:Muscle, Skeletal / Q000276:immunology / Q000473:pathology*; D017285:Polymyositis / Q000276:immunology / Q000473:pathology*; D011956:Receptors, Cell Surface / Q000378:metabolism; D016176:T-Lymphocyte Subsets / Q000473:pathology; D000098902:CD163 Antigen
D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000098902:CD163 Antigen; D017252:CD3 Complex; D006684:HLA-DR Antigens; D015395:Histocompatibility Antigens Class I; D053582:Interleukin-1alpha; D011956:Receptors, Cell Surface