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Discordant Gene and Surface Expression of the T-Cell Receptor/CD3 Complex in Adult T-Cell Leukemia Cells¹

Second Department of Internal Medicine, Kumamoto University Medical School, 1-1-1 Honjo, Kumamoto 860, Japan [H. S., T. S., N. A., J-x. W., K. N., T. O., K. T.], and Division of Tumor Immunology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115 [P.A.]

Cell surface expression of the T-cell receptor (TCR)/CD3 complex on the cells from 11 acute type adult T-cell leukemia (ATL) and 4 lymphoma type ATL patients was examined by flow cytometry. Cells from 10 of 11 acute ATL patients were TCR ß+ and CD3+, and their mean fluorescence intensities were low (TCRß, 25.3–84.6; CD3, 22.8–87.8). Cells from two of four lymphoma type ATL did not express this complex, and the other two were CD3+, TCR ß-. In contrast, the mean fluorescence intensity of the TCR/CD3 complex in cells from a patient with T4 chronic lymphocytic leukemia was not low (TCR ß, 129.9; CD3, 117.1). mRNA expressions of the TCR , ß, and CD3 , , , and chains were examined by Northern blots. ATL cells from two acute and two lymphoma types expressed amounts of this complex equal to or greater than those expressed by T4 chronic lymphocytic leukemia. CD3 and TCR ß mRNA in ATL and T4 chronic lymphocytic leukemia cells were equally stable to actinomycin D treatment. The synthesis of CD3 protein by ATL cells was detected by Western blotting assay. On the basis of these findings, we discuss the possible involvement of the TCR/CD3 complex in activation of ATL cells.

¹ This work was supported by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science and Culture of Japan, and Science Research expenses for Health and Welfare Programs from the Ministry of Health and Welfare, Japan.

² To whom requests for reprints should be addressed.

Received 6/20/91. Accepted 9/11/91.

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