Identification of biclonal (duplex) leukaemic cells expressing either CD4+/CD8- or CD4-/CD8+ from a patient with adult T-cell leukaemia/lymphoma.
ABSTRACT A 24-year-old Japanese woman was admitted to our hospital in 1987 with a chief complaint of skin eruptions, and was diagnosed as having chronic ATLL. In 1993 the leucocyte count increased gradually to 126.0 x 10(9)/l with 91.5% abnormal lymphocytes expressing two different types of antigenicity, either CD+/CD8- or CD4-/CD8+. Monoclonal integration of human T-cell lymphotropic virus type-I proviral DNA was detected at different sites of the genomic DNA in each cell type. These studies clearly indicate that CD4+/CD8- and CD4-/CD8+ leukaemic cells originated from two independent clones.
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ABSTRACT: Typical adult T-cell leukaemia (ATL) cells have a CD4+ CD8- cell surface phenotype, but atypical phenotypes such as CD4+ CD8+ and CD4- CD8+ have also been reported. The CD8 molecule is composed of alpha and beta chains and commonly used monoclonal antibodies against CD8 molecule detect only CD8alpha. Since it has been reported that CD8alpha can be induced in mature CD4+ T cells by cell activation, but not CD8beta, we studied whether ATL cells which express CD8alpha may also express CD8beta. We found some cases of CD8alpha+ ATL were also positive for CD8beta. Furthermore, we experienced a case whose ATL cell surface phenotype changed from CD4+ CD8alpha+ CD8beta+ to CD4- CD8alpha+ CD8beta+ and finally to CD4+ CD8alpha- CD8beta-. Southern blot analysis revealed that the monoclonal integration of human T lymphotropic virus type I (HTLV-I) was identical throughout the course of the study, indicating that a single clone had demonstrated the alterations. These data suggest that peripheral CD4+ CD8+ ATL cells can express not only CD8alpha, but also CD8beta and that a single ATL cell clone has the potential to change its surface phenotype in vivo as well as in vitro.British Journal of Haematology 08/1997; 98(1):151-6. · 4.96 Impact Factor
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ABSTRACT: In this review, we discuss the possible relationship between the clinical characteristics and the multiple integration of human T-cell lymphotropic virus type I (HTLV-I) proviral DNA in patients with adult T-cell leukemia/lymphoma (ATL). Some patients with ATL show multiple HTLV-I integrations and exhibit clinical characteristics unlike those of ATL patients who show the typical integration of a single provirus. Multiple HTLV-I integrations can be detected by Southern blotting as multiple bands having varied intensities. These multiple integration conditions can arise from one tumor cell clone carrying multiple copies of the provirus, or from multiple cell clones, each carrying one copy of the provirus. The former patients manifest an extremely aggressive clinical course with the infiltration of unusual organs such as the retina and uvea. The latter patients show an indolent clinical course with skin lesions. These findings suggest that the clinical implications for multiple HTLV-I integrations exist in ATL. This may be one of the explanations for the heterogeneous findings in the disease. Such observations may provide information linking viral integration with clinical manifestations, and improve our understanding of the pathogenesis of ATL.Leukemia and Lymphoma 10/1997; 27(1-2):43-51. · 2.61 Impact Factor
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ABSTRACT: The association of CD26/dipeptidyl peptidase IV (DPPIV) and human T lymphotropic virus type I (HTLV-I) was studied by two approaches. First, we examined the expression of CD26 in peripheral blood mononuclear cells (PBMC) from the patients with adult T cell leukemia/lymphoma (ATLL), an HTLV-I-related malignancy. The expression of CD26 on the surface of PBMC was decreased in all 20 patients with ATLL compared with those from normal individuals (P < 0.01) and the expression of the CD26 gene transcript was not detectable in seven out of eight patients with ATLL. Then we compared the quantity of viral DNA in CD26-negative (CD26-) and CD26-positive (CD26+) cells obtained from 17 HTLV-I healthy carries by using a polymerase chain reaction method. The CD26-cells had a higher copy number of viral DNA than CD26+ cells. These findings indicate that HTLV-I has in vivo tropism to CD26- cells, suggesting that some phenotypes of ATLL cells reflect the in vivo cellular tropism of HTLV-I.Leukemia Research 04/1996; 20(4):357-63. · 2.69 Impact Factor