Associations with autoimmune disorders and HLA class I and II antigens in inclusion body myositis

Whether autoimmune mechanisms play a role in the pathogenesis of inclusion body myositis (IBM) is unknown. Human leukocyte antigen (HLA) analysis in 52 patients, including 17 with autoimmune disorders (AIDs), showed that patients were more likely to have antigens from the autoimmune-prone HLA-B8-DR3...

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Veröffentlicht in:	Neurology 2004-12, Vol.63 (12), p.2396-2398
Hauptverfasser:	BADRISING, U. A, SCHREUDER, G. M. Th, GIPHART, M. J, GELEIJNS, K, VERSCHUUREN, J. J. G. M, WINTZEN, A. R
Format:	Artikel
Sprache:	eng
Schlagworte:	Age of Onset Aged Aged, 80 and over Autoimmune Diseases - epidemiology Autoimmune Diseases - genetics Autoimmune Diseases - immunology Biological and medical sciences Comorbidity Diseases of striated muscles. Neuromuscular diseases Female Gene Frequency Genes, MHC Class I Genes, MHC Class II Genetic Predisposition to Disease Haplotypes - genetics HLA Antigens - analysis HLA Antigens - genetics HLA Antigens - immunology HLA-D Antigens - analysis HLA-D Antigens - genetics HLA-D Antigens - immunology HLA-DR Antigens - analysis HLA-DR Antigens - genetics HLA-DR Antigens - immunology HLA-DRB4 Chains Humans Male Medical sciences Middle Aged Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis Myositis, Inclusion Body - epidemiology Myositis, Inclusion Body - genetics Myositis, Inclusion Body - immunology Netherlands - epidemiology Neurology Prevalence
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Beschreibung
Zusammenfassung:	Whether autoimmune mechanisms play a role in the pathogenesis of inclusion body myositis (IBM) is unknown. Human leukocyte antigen (HLA) analysis in 52 patients, including 17 with autoimmune disorders (AIDs), showed that patients were more likely to have antigens from the autoimmune-prone HLA-B8-DR3 ancestral haplotype than healthy control subjects, irrespective of the presence of AIDs. Patients lacked the apparently protective HLA-DR53 antigen. The results provide further support for an autoimmune basis in IBM.
ISSN:	0028-3878 1526-632X
DOI:	10.1212/01.WNL.0000148588.15052.4C