Volume 52, Issue 1 pp. 1-7
Original Article
Free Access

Random suppression of T cells that bear specific T cell receptor Vβ sequences in adult T cell leukemia/lymphoma (ATLL) patients at each clinical stage: Carrier, smoldering, chronic, and acute

Koichi Ohshima

Corresponding Author

Koichi Ohshima

Department of Pathology, and First Internal Medicine, School of Medicine, Fukuoka University, Fukuoka, Japan

Department of Pathology, School of Medicine, Fukuoka University, Nanakuma 7-45-1, Jonan-ku, Fukuoka 814-01, JapanSearch for more papers by this author
Junji Suzumiya

Junji Suzumiya

Department of Pathology, and First Internal Medicine, School of Medicine, Fukuoka University, Fukuoka, Japan

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Masahiro Kikuchi

Masahiro Kikuchi

Department of Pathology, and First Internal Medicine, School of Medicine, Fukuoka University, Fukuoka, Japan

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Morishige Takeshita

Morishige Takeshita

Department of Pathology, and First Internal Medicine, School of Medicine, Fukuoka University, Fukuoka, Japan

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Kotaro Tashiro

Kotaro Tashiro

Department of Pathology, and First Internal Medicine, School of Medicine, Fukuoka University, Fukuoka, Japan

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Nobuhiro Kimura

Nobuhiro Kimura

Department of Pathology, and First Internal Medicine, School of Medicine, Fukuoka University, Fukuoka, Japan

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Abstract

Human T cell leukemia virus type I (HTLV-I) is associated with adult T cell leukemia/lymphoma (ATLL), which is well known as a T cell malignancy. In order to clarify whether HTLV-I plays a role as a virus-encoded superantigen in the neoplastic process, we examined the TCR Vβ families in the peripheral blood at four different clinical stages: carrier, smoldering leukemia, chronic leukemia, and acute leukemia. An increased number of CD4 T cells was found in each of the four clinical stages. However, we found neither uniform specific losses nor uniform clonal expansion of particular TCR Vβ gene families in any case from the four clinical stages. However, a suppression of the random TCR Vβ families was found. Our data did not therefore directly suggest the existence of a common superantigen model of HTLV-I which induces an increase in CD4 T cells. The random suppression in the TCR Vβ repertoire is most likely caused by the influence of HTLV-I neoplastic pathogenesis rather than by virus-encoded superantigens. In the patients with acute leukemia, one or two families of the Vβ repertoires were very strongly expressed, while in chronic leukemia, no such repertoire of strong expression was observed. The immunological reaction of the hosts might thus be different between the above described groups. © 1996 Wiley-Liss, Inc.

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