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Research Article Free access | 10.1172/JCI119100

HLA-B27 heavy chains contribute to spontaneous inflammatory disease in B27/human beta2-microglobulin (beta2m) double transgenic mice with disrupted mouse beta2m.

S D Khare, J Hansen, H S Luthra, and C S David

Department of Immunology, Mayo Clinic and Medical School, Rochester, Minnesota 55905, USA.

Find articles by Khare, S. in: JCI | PubMed | Google Scholar

Department of Immunology, Mayo Clinic and Medical School, Rochester, Minnesota 55905, USA.

Find articles by Hansen, J. in: JCI | PubMed | Google Scholar

Department of Immunology, Mayo Clinic and Medical School, Rochester, Minnesota 55905, USA.

Find articles by Luthra, H. in: JCI | PubMed | Google Scholar

Department of Immunology, Mayo Clinic and Medical School, Rochester, Minnesota 55905, USA.

Find articles by David, C. in: JCI | PubMed | Google Scholar

Published December 15, 1996 - More info

Published in Volume 98, Issue 12 on December 15, 1996
J Clin Invest. 1996;98(12):2746–2755. https://doi.org/10.1172/JCI119100.
© 1996 The American Society for Clinical Investigation
Published December 15, 1996 - Version history
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Abstract

MHC class I allele, HLA-B27, is strongly associated with a group of human diseases called spondyloarthropathies. Some of these diseases have an onset after an enteric or genitourinary infection. In the present study, we describe spontaneous disease in HLA-B27 transgenic mice where endogenous beta2-microglobulin (beta2m) gene was replaced with transgenic human beta2m gene. These mice showed cell surface expression of HLA-B27 similar to that of human peripheral blood mononuclear cells. In addition, free heavy chains (HCs) of HLA-B27 were also expressed on thymic epithelium and on a subpopulation of B27-expressing PBLs. These mice developed spontaneous arthritis and nail changes in the rear paws. Arthritis occurred primarily in male animals and only when mice were transferred from the pathogen-free barrier facility to the conventional area. Transgenic mice expressing HLA-B27 with mouse beta2m have undetectable levels of free HCs on the cell surface and do not develop arthritis. In vivo treatment with anti-HC-specific antibody delayed the onset of disease. Our data demonstrate specific involvement of HLA-B27 'free' HCs in the disease process.

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