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Research Article Free access | 10.1172/JCI113524

T cell receptor beta chain gene rearrangement shared by murine T cell lines derived from a site of autoimmune inflammation.

S J Padula, D C Sgroi, E G Lingenheld, J T Love Jr, C H Chou, and R B Clark

Department of Medicine, University of Connecticut School of Medicine, Farmington 06032.

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

Department of Medicine, University of Connecticut School of Medicine, Farmington 06032.

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Department of Medicine, University of Connecticut School of Medicine, Farmington 06032.

Find articles by Lingenheld, E. in: JCI | PubMed | Google Scholar

Department of Medicine, University of Connecticut School of Medicine, Farmington 06032.

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

Department of Medicine, University of Connecticut School of Medicine, Farmington 06032.

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

Department of Medicine, University of Connecticut School of Medicine, Farmington 06032.

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Published June 1, 1988 - More info

Published in Volume 81, Issue 6 on June 1, 1988
J Clin Invest. 1988;81(6):1810–1818. https://doi.org/10.1172/JCI113524.
© 1988 The American Society for Clinical Investigation
Published June 1, 1988 - Version history
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Abstract

Advances in our understanding of the structure and molecular biology of the T lymphocyte antigen-receptor have now made it feasible to study human autoimmune diseases using new approaches. One such approach involves cloning of T cells from sites of autoimmune pathology followed by identification of putative disease-related T cell oligoclonality at the level of the T cell receptor gene rearrangements. We have now tested the feasibility of this approach in an animal model of autoimmunity, murine experimental allergic encephalomyelitis (EAE). Spinal cord-derived, self (murine) myelin basic protein (MBP)-reactive T cell lines and sublines were analyzed at the level of their receptor beta chain rearrangements using Southern blots. We now report that the MBP-reactive T cell lines and sublines derived from the spinal cords of four of five SJL/J mice with EAE share a 14.5-kb rearranged T cell receptor beta 1 band on Southern blots. A spinal cord-derived T cell line that was reactive to purified protein derivative of tuberculin (PPD), several lymph node-derived ovalbumin- and PPD-reactive T cell lines, as well as one MBP-reactive spinal cord-derived T cell line did not share this 14.5-kb rearranged beta 1 band. These results suggest that analysis of the antigen receptors used by T cells cloned from sites of inflammation may be a useful initial approach for identifying pathogenetically relevant T cells in the study of certain human autoimmune diseases.

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