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Research Article Free access | 10.1172/JCI118921

Selective expansion of specific T cell receptors in the inflamed colon of Crohn's disease.

B Gulwani-Akolkar, P N Akolkar, A Minassian, R Pergolizzi, M McKinley, G Mullin, S Fisher, and J Silver

Department of Medicine, North Shore University Hospital/Cornell University Medical College, Manhasset, New York 11030, USA.

Find articles by Gulwani-Akolkar, B. in: JCI | PubMed | Google Scholar

Department of Medicine, North Shore University Hospital/Cornell University Medical College, Manhasset, New York 11030, USA.

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Department of Medicine, North Shore University Hospital/Cornell University Medical College, Manhasset, New York 11030, USA.

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Department of Medicine, North Shore University Hospital/Cornell University Medical College, Manhasset, New York 11030, USA.

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Department of Medicine, North Shore University Hospital/Cornell University Medical College, Manhasset, New York 11030, USA.

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Department of Medicine, North Shore University Hospital/Cornell University Medical College, Manhasset, New York 11030, USA.

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Department of Medicine, North Shore University Hospital/Cornell University Medical College, Manhasset, New York 11030, USA.

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Department of Medicine, North Shore University Hospital/Cornell University Medical College, Manhasset, New York 11030, USA.

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Published September 15, 1996 - More info

Published in Volume 98, Issue 6 on September 15, 1996
J Clin Invest. 1996;98(6):1344–1354. https://doi.org/10.1172/JCI118921.
© 1996 The American Society for Clinical Investigation
Published September 15, 1996 - Version history
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Abstract

To identify disease-specific T cell changes that occur in Crohn's disease (CD), the T cell receptor BV repertoires of lamina propria lymphocytes (LPL) isolated from both the inflamed and "disease-inactive" colons of seven CD patients were compared by the quantitative PCR and DNA sequence analysis. It was observed that the BV repertoires of LPL isolated from the disease-active and disease-inactive parts of the colon from the same individual were very different. Furthermore, nearly all of the differences occurred in CD4+ LPL, with very few differences in the CD8+ population of LPL. Although the pattern of BV segments that was increased in disease-active tissue relative to disease-inactive tissue was different for all seven CD patients, there were several BV segments that increased uniformly in the disease-active tissue of all seven individuals. CDR3 length analysis and DNA sequencing of these BV segments revealed that in six of the seven CD patients there was a striking degree of oligoclonality that was absent from disease-inactive tissue of the same individual. These observations suggest that at least some of the inflammation in CD is the result of responses by CD4+ T cells to specific antigens. The isolation of such inflammation-specific CD4+ T cells may make it possible to identify the antigens that are responsible for the inflammatory process in CD and provide a better understanding of its pathogenesis.

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  • Version 1 (September 15, 1996): No description

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