Badrising U A, Schreuder G M Th, Giphart M J, Geleijns K, Verschuuren J J G M, Wintzen A R, Maat-Schieman M L C, van Doorn P, van Engelen B G M, Faber C G, Hoogendijk J E, de Jager A E, Koehler P J, de Visser M, van Duinen S G
Department of Neurology, K5Q, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands.
Neurology. 2004 Dec 28;63(12):2396-8. doi: 10.1212/01.wnl.0000148588.15052.4c.
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.
自身免疫机制是否在包涵体肌炎(IBM)的发病机制中起作用尚不清楚。对52例患者进行的人类白细胞抗原(HLA)分析,其中包括17例自身免疫性疾病(AIDs)患者,结果显示,无论是否患有AIDs,患者比健康对照受试者更有可能拥有来自易患自身免疫性疾病的HLA - B8 - DR3祖传单倍型的抗原。患者缺乏明显具有保护作用的HLA - DR53抗原。这些结果为IBM的自身免疫基础提供了进一步的支持。