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The Journal of Immunology, 2000, 164: 2823-2831.
Copyright © 2000 by The American Association of Immunologists

Accumulation of Common T Cell Clonotypes in the Salivary Glands of Patients with Human T Lymphotropic Virus Type I-Associated and Idiopathic Sjögren’s Syndrome1

Masanori Sasaki*, Seiji Nakamura2,*, Yukiko Ohyama*, Masanori Shinohara*, Ichiko Ezaki{dagger}, Hideo Hara{ddagger}, Tsutomu Kadena*, Kenji Kishihara§, Kazuhiko Yamamoto, Kikuo Nomoto§ and Kanemitsu Shirasuna*

* Second Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, Kyushu University, Fukuoka, Japan; {dagger} Department of Food and Nutrition, Beppu University Junior College, Beppu, Oita, Japan; {ddagger} Department of Neurology and Neuropathology, Neurological Institute, Faculty of Medicine, Kyushu University, Fukuoka, Japan; § Department of Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan; and Department of Allergy and Rheumatology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan


   Abstract
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To clarify the pathogenesis of human T lymphotropic virus type I (HTLV-I)-associated Sjögren’s syndrome (SS), the TCR Vß gene usage by the infiltrating lymphocytes in the target organ was examined. The Vß families predominantly used in the labial salivary gland (LSG) from the HTLV-I-seropositive (HTLV-I+) SS patients were more restricted than those from the HTLV-I-seronegative (idiopathic) SS patients, and were commonly Vß5.2, Vß6, and Vß7. The single-strand conformation polymorphism analysis revealed that T cell clonotypes with Vß5.2, Vß6, and Vß7 accumulate in the LSG from the HTLV-I+ and idiopathic SS patients. Among junctional sequences of the most dominant Vß7 transcripts, the conserved amino acid motif (QDXG: X is any amino acid) was found in six of the five HTLV-I+ SS patients and was also detected in two of the five idiopathic SS patients. Using the probes specific to the motif, the Vß7 transcripts with the motif were detected in the LSG from all of the seven HTLV-I+ and five of the six idiopathic SS patients, but not from eight healthy subjects. The Vß7 transcripts with this motif were also detected in the HTLV-I-infected T cell lines obtained from the LSG of an HTLV-I+ SS patient. The accumulation of HTLV-I-infected T cells expressing TCR with the conserved motif was thus indicated. These T cells were commonly present in patients with idiopathic SS and are strongly suggested to most likely be involved in the pathogenesis of both HTLV-I-associated and idiopathic SS.


   Acknowledgments
 
We thank Dr. S. M. Fu for his valuable discussions, and Dr. B. T. Quinn for his critical review of the manuscript.

Received for publication June 1, 1999. Accepted for publication December 20, 1999.


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