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Monoclonal proliferation of double‐negative (CD4 − CD8 − ) T‐cells bearing T‐Cell receptor‐αβ followed by subsequent development of Hodgkin's disease
Author(s) -
Matsumoto Mitsuru,
Takada Kiyonori,
Hato Takaaki,
Horiuchi Takahiko,
Yasukawa Masaki,
Murao Shinichi,
Fujita Shigeru
Publication year - 1994
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(19940601)73:11<2818::aid-cncr2820731126>3.0.co;2-l
Subject(s) - cd8 , t cell receptor , double negative , cytotoxic t cell , t cell , monoclonal antibody , immunology , medicine , monoclonal , lymphoproliferative disorders , cd3 , t lymphocyte , cancer research , biology , lymphoma , antigen , immune system , antibody , in vitro , genetics
Abstract Expression of CD4 or CD8 on the cell surface is an important guide for discriminating the immunologic functions of T‐cells. However, a minor T‐cell subset lacking both CD4 and CD8 molecules but bearing the usual form of T‐cell receptor (TCR)‐αβ (CD4 − CD8 − TCR‐αβ + T‐cells) has recently been found not only in mice but also in humans, and the clinical relevance of this newly defined subpopulation to human diseases is now of considerable interest. The authors present a patient in whom CD4 − CD8 − TCR‐αβ + T‐cells showed monoclonal proliferation in the peripheral blood for more than 3 years, then disappeared spontaneously, followed by subsequent development of Hodgkin's disease. The pathologic roles of double‐negative T‐cell proliferation in this case are discussed from the viewpoint of premalignancy in lymphoproliferative diseases. Cancer 1994; 73:2818–23.