Functional and phenotypic comparison of human T cell leukemia/lymphoma virus positive adult T cell leukemia with human T cell leukemia/lymphoma virus negative Sézary leukemia, and their distinction using anti-Tac. Monoclonal antibody identifying the human receptor for T cell growth factor
T A Waldmann, W C Greene, P S Sarin, C Saxinger, D W Blayney, W A Blattner, C K Goldman, K Bongiovanni, S Sharrow, J M Depper, T A Waldmann, W C Greene, P S Sarin, C Saxinger, D W Blayney, W A Blattner, C K Goldman, K Bongiovanni, S Sharrow, J M Depper
Abstract
Adult T cell leukemia (ATL) and Sézary leukemia are malignant proliferations of T lymphocytes that share similar cell morphology and clinical features. ATL is associated with HTLV (human T cell leukemia/lymphoma virus), a unique human type C retrovirus, whereas most patients with the Sézary syndrome do not have antibodies to this virus. Leukemic cells of both groups were of the T3, T4-positive, T8-negative phenotype. Despite the similar phenotype, HTLV-negative Sézary leukemic cells frequently functioned as helper cells, whereas some HTLV-positive ATL and HTLV-positive Sézary cells appeared to function as suppressors of immunoglobulin synthesis. One can distinguish the HTLV-positive from the HTLV-negative leukemias using a monoclonal antibody (anti-Tac) that appears to identify the human receptor for T cell growth factor (TCGF). Resting normal T cells and most HTLV-negative Sézary cells were Tac-negative, whereas all ATL cell populations were Tac-positive. The observation that ATL cells manifest TCGF receptors suggests the possibility that an abnormality of the TCGF-TCGF receptor system may partially explain the uncontrolled growth of these cells.
References
- Science. 1976 Sep 10;193(4257):1007-8
- Proc Natl Acad Sci U S A. 1982 Sep;79(18):5680-3
- Nature. 1982 Nov 18;300(5889):267-9
- Virology. 1982 Oct 30;122(2):297-305
- J Exp Med. 1982 Oct 1;156(4):1065-76
- Science. 1983 Feb 18;219(4586):856-9
- J Infect Dis. 1983 Mar;147(3):406-16
- JAMA. 1983 Aug 26;250(8):1048-52
- Nature. 1983 Oct 20-26;305(5936):733-6
- Proc Natl Acad Sci U S A. 1983 Nov;80(22):6957-61
- Acta Pathol Jpn. 1982;32 Suppl 1:171-85
- J Immunol. 1976 Nov;117(5 Pt 1):1538-44
- Blood. 1977 Sep;50(3):481-92
- N Engl J Med. 1978 Jan 12;298(2):66-72
- Clin Immunol Immunopathol. 1978 May;10(1):24-34
- N Engl J Med. 1978 Dec 7;299(23):1281-4
- Nature. 1979 Feb 8;277(5696):478-80
- Blood. 1979 Apr;53(4):642-51
- Clin Immunol Immunopathol. 1979 Mar;12(3):341-50
- Proc Natl Acad Sci U S A. 1979 Aug;76(8):4061-5
- J Immunol. 1980 Mar;124(3):1301-7
- Proc Natl Acad Sci U S A. 1980 Mar;77(3):1588-92
- Immunol Rev. 1979;47:3-61
- Clin Immunol Immunopathol. 1980 Sep;17(1):43-54
- J Immunol. 1981 Apr;126(4):1393-7
- J Immunol. 1981 Apr;126(4):1398-403
- Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9
- Cell. 1981 Mar;23(3):771-80
- J Exp Med. 1981 Jul 1;154(1):156-67
- J Exp Med. 1981 Aug 1;154(2):459-67
- Proc Natl Acad Sci U S A. 1981 Jul;78(7):4515-9
- Nature. 1981 Nov 19;294(5838):268-71
- Nature. 1981 Nov 19;294(5838):271-3
- Proc Natl Acad Sci U S A. 1981 Oct;78(10):6476-80
- J Immunol. 1982 Aug;129(2):592-5
- Proc Natl Acad Sci U S A. 1982 Apr;79(7):2365-9
- Blood. 1982 Sep;60(3):545-57
- Adv Immunol. 1982;32:1-63
- Science. 1982 Oct 29;218(4571):471-3
- Int J Cancer. 1982 Sep 15;30(3):257-64
- J Clin Invest. 1976 Dec;58(6):1297-306
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