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Amendment history:
  • Correction (July 1992)

Research Article Free access | 10.1172/JCI115635

T cell receptor repertoire of infiltrating T cells in lips of Sjögren's syndrome patients.

T Sumida, F Yonaha, T Maeda, E Tanabe, T Koike, H Tomioka, and S Yoshida

Second Department of Internal Medicine, School of Medicine, Chiba University, Japan.

Find articles by Sumida, T. in: JCI | PubMed | Google Scholar

Second Department of Internal Medicine, School of Medicine, Chiba University, Japan.

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Second Department of Internal Medicine, School of Medicine, Chiba University, Japan.

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Second Department of Internal Medicine, School of Medicine, Chiba University, Japan.

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Second Department of Internal Medicine, School of Medicine, Chiba University, Japan.

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Second Department of Internal Medicine, School of Medicine, Chiba University, Japan.

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Second Department of Internal Medicine, School of Medicine, Chiba University, Japan.

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Published February 1, 1992 - More info

Published in Volume 89, Issue 2 on February 1, 1992
J Clin Invest. 1992;89(2):681–685. https://doi.org/10.1172/JCI115635.
© 1992 The American Society for Clinical Investigation
Published February 1, 1992 - Version history
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Abstract

Infiltrating T cells around salivary glands in the lips of Sjögren's syndrome (SjS) patients are crucial in the pathogenesis of this disease. To analyze the nature of infiltrating T cells, their T cell receptor repertoire was examined with quantitative polymerase chain reaction. The repertoire of V beta transcripts in lips of SjS was not restricted; however, the V beta 2 and V beta 13 genes were predominantly expressed on the T cells of lip specimens in six and four of seven lips, respectively. Predominance of these genes was specific in lips because no predominant V beta transcripts were found in lips from healthy subjects and PBLs from SjS patients. These results indicated that the V beta 2- and V beta 13-positive T cells expanded specifically and preferentially in SjS lips, thereby suggesting the possible role in triggering the autoimmunity of this disease.

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