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Rheumatology Advance Access originally published online on October 27, 2004
Rheumatology 2005 44(2):192-196; doi:10.1093/rheumatology/keh449
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Rheumatology Vol. 44 No. 2 © British Society for Rheumatology 2004; all rights reserved

Lack of circulating autoantibodies to bone morphogenetic protein receptor-II or activin receptor-like kinase 1 in mixed connective tissue disease patients with pulmonary arterial hypertension

T. Satoh1,3, K. Kimura1, Y. Okano4, M. Hirakata2, Y. Kawakami1 and M. Kuwana

1 Institute for Advanced Medical Research, Keio University School of Medicine and 2 Department of Internal Medicine, Keio University School of Medicine, Tokyo, 3 Department of Laboratory Medicine, Kitasato University Graduate School of Medical Sciences, Sagamihara and 4 Okano Clinic, Abiko, Japan.

Correspondence to: M. Kuwana, Institute for Advanced Medical Research, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. E-mail: kuwanam{at}sc.itc.keio.ac.jp

Objectives. To examine whether autoantibodies against bone morphogenetic protein receptor-II (BMPR-II) or activin receptor-like kinase 1 (ALK-1) are associated with pulmonary arterial hypertension (PAH) in patients with mixed connective tissue disease (MCTD).

Methods. We studied sera from 37 MCTD patients with or without PAH, six patients with idiopathic PAH, and 30 healthy controls. Circulating anti-BMPR-II and anti-ALK-1 antibodies were detected using immunoprecipitation of recombinant antigens generated by in vitro transcription/translation and indirect immunofluorescence of cultured cells that were induced to express these antigens by gene transfer. Anti-BMPR-II antibodies were further examined by immunoprecipitation and immunoblotting using a recombinant fragment of the extracellular domain of BMPR-II.

Results. Serum anti-BMPR-II and anti-ALK-1 autoantibodies were not detected in MCTD patients irrespective of the presence or absence of PAH, or in patients with idiopathic PAH.

Conclusions. Our finding does not support the hypothesis that autoantibody-mediated dysregulation of signals through BMPR-II or ALK-1 contributes to the development of PAH in patients with connective tissue diseases.

KEY WORDS: Pulmonary arterial hypertension, Autoantibody, Mixed connective tissue disease, Bone morphogenetic protein receptor-II, Activin receptor-like kinase 1


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