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Research Article Free access | 10.1172/JCI117801

Juvenile chronic arthritis: T cell reactivity to human HSP60 in patients with a favorable course of arthritis.

E R de Graeff-Meeder, W van Eden, G T Rijkers, B J Prakken, W Kuis, M M Voorhorst-Ogink, R van der Zee, H J Schuurman, P J Helders, and B J Zegers

Department of Immunology, University Hospital for Children and Youth Het Wilhelmina Kinderziekenhuts, Utrecht, The Netherlands.

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Department of Immunology, University Hospital for Children and Youth Het Wilhelmina Kinderziekenhuts, Utrecht, The Netherlands.

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Department of Immunology, University Hospital for Children and Youth Het Wilhelmina Kinderziekenhuts, Utrecht, The Netherlands.

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Department of Immunology, University Hospital for Children and Youth Het Wilhelmina Kinderziekenhuts, Utrecht, The Netherlands.

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Department of Immunology, University Hospital for Children and Youth Het Wilhelmina Kinderziekenhuts, Utrecht, The Netherlands.

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Department of Immunology, University Hospital for Children and Youth Het Wilhelmina Kinderziekenhuts, Utrecht, The Netherlands.

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Department of Immunology, University Hospital for Children and Youth Het Wilhelmina Kinderziekenhuts, Utrecht, The Netherlands.

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Department of Immunology, University Hospital for Children and Youth Het Wilhelmina Kinderziekenhuts, Utrecht, The Netherlands.

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Department of Immunology, University Hospital for Children and Youth Het Wilhelmina Kinderziekenhuts, Utrecht, The Netherlands.

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Department of Immunology, University Hospital for Children and Youth Het Wilhelmina Kinderziekenhuts, Utrecht, The Netherlands.

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Published March 1, 1995 - More info

Published in Volume 95, Issue 3 on March 1, 1995
J Clin Invest. 1995;95(3):934–940. https://doi.org/10.1172/JCI117801.
© 1995 The American Society for Clinical Investigation
Published March 1, 1995 - Version history
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Abstract

Synovial fluid and peripheral blood mononuclear cell proliferative responses to the 60-kD human heat shock protein (HSP60) were studied in 23 patients with juvenile chronic arthritis (JCA) and 7 non-JCA control patients. All patients showed active arthritis at the time of study. The patients were divided into two groups according to the presence (group A) or absence (group B) of T lymphocyte reactivity to human HSP60. We show that reactivity to human HSP60 is primarily, though not exclusively, occurring in patients with a remitting course of disease, i.e., the subgroup of HLA-B27 negative JCA patients with an oligoarticular onset. Immunohistochemical analysis of HSP expression in synovial membranes showed a significantly higher intensity of staining in JCA patients than in non-JCA controls. The results suggest that, in accordance with the earlier observation made in experimental models, T lymphocyte reactivity to human HSP60 in this subgroup of JCA patients may be part of T cell regulatory mechanisms that control the development of arthritis.

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