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

U. A. Badrising; G. M. Th Schreuder; M. J. Giphart; K. Geleijns; J. J. G. M. Verschuuren; A. R. Wintzen; M. L. C. Maat-Schieman; P. van Doorn; B. G. M. van Engelen; C. G. Faber; J. E. Hoogendijk; A. E. de Jager; P. J. Koehler; M. de Visser; S. G. van Duinen

doi:https://doi.org/10.1212/01.WNL.0000148588.15052.4C

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

U. A. Badrising, G. M. Th Schreuder, M. J. Giphart, K. Geleijns, J. J. G. M. Verschuuren, A. R. Wintzen, M. L. C. Maat-Schieman, P. van Doorn, B. G. M. van Engelen, C. G. Faber, J. E. Hoogendijk, A. E. de Jager, P. J. Koehler, M. de Visser, S. G. van Duinen

Neurology (AMC)

Research output: Contribution to journal › Article › Academic › peer-review

92 Citations (Scopus)

Abstract

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

Original language	English
Pages (from-to)	2396-2398
Journal	Neurology
Volume	63
Issue number	12
DOIs	https://doi.org/10.1212/01.WNL.0000148588.15052.4C
Publication status	Published - 2004

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https://doi.org/10.1212/01.WNL.0000148588.15052.4C

Cite this

Badrising, U. A., Schreuder, G. M. T., 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. (2004). Associations with autoimmune disorders and HLA class I and II antigens in inclusion body myositis. Neurology, 63(12), 2396-2398. https://doi.org/10.1212/01.WNL.0000148588.15052.4C

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title = "Associations with autoimmune disorders and HLA class I and II antigens in inclusion body myositis",

abstract = "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",

author = "Badrising, {U. A.} and Schreuder, {G. M. Th} and Giphart, {M. J.} and K. Geleijns and Verschuuren, {J. J. G. M.} and Wintzen, {A. R.} and Maat-Schieman, {M. L. C.} and {van Doorn}, P. and {van Engelen}, {B. G. M.} and Faber, {C. G.} and Hoogendijk, {J. E.} and {de Jager}, {A. E.} and Koehler, {P. J.} and {de Visser}, M. and {van Duinen}, {S. G.}",

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Badrising, UA, Schreuder, GMT, Giphart, MJ, Geleijns, K, Verschuuren, JJGM, Wintzen, AR, Maat-Schieman, MLC, van Doorn, P, van Engelen, BGM, Faber, CG, Hoogendijk, JE, de Jager, AE, Koehler, PJ, de Visser, M & van Duinen, SG 2004, 'Associations with autoimmune disorders and HLA class I and II antigens in inclusion body myositis', Neurology, vol. 63, no. 12, pp. 2396-2398. https://doi.org/10.1212/01.WNL.0000148588.15052.4C

TY - JOUR

T1 - Associations with autoimmune disorders and HLA class I and II antigens in inclusion body myositis

AU - Badrising, U. A.

AU - Schreuder, G. M. Th

AU - Giphart, M. J.

AU - Geleijns, K.

AU - Verschuuren, J. J. G. M.

AU - Wintzen, A. R.

AU - Maat-Schieman, M. L. C.

AU - van Doorn, P.

AU - van Engelen, B. G. M.

AU - Faber, C. G.

AU - Hoogendijk, J. E.

AU - de Jager, A. E.

AU - Koehler, P. J.

AU - de Visser, M.

AU - van Duinen, S. G.

PY - 2004

Y1 - 2004

N2 - 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

AB - 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

U2 - https://doi.org/10.1212/01.WNL.0000148588.15052.4C

DO - https://doi.org/10.1212/01.WNL.0000148588.15052.4C

M3 - Article

C2 - 15623710

SN - 0028-3878

VL - 63

SP - 2396

EP - 2398

JO - Neurology

JF - Neurology

IS - 12

ER -