Important note: Information in this article was accurate in 1994. The state of the art may have changed since the publication date.
Expression of the target antigen for cytotoxic T lymphocytes on adult T cell leukemia cells (Meeting abstract).
International Association for Comparative Research on Leukemia and Related Diseases, 16th Symposium. July 11-16, 1993, Montreal, Quebec, Canada, A57, 1993.. Unique Identifier : AIDSLINE ICDB/94698655 Kannagi M; Matsushita S; Harada S; Kumamoto Univ. Sch. of Medicine, Kumamoto, Japan
Abstract:
Human T-cell leukemia virus type-I (HTLV-I) persistently infects human T lymphocytes, and is associated with both malignant and inflammatory diseases. HTLV-I-specific cytotoxic T lymphocytes (CTL) are considered to contribute to in vivo surveillance and elimination of HTLV-I-infected cells. HTLV-I-specific CTL can be frequently induced from peripheral blood lymphocytes of patients with HTLV-I-related disorders including HTLV-I associated myelopathy and tropical spastic paraparesis (HAM/TSP), but not from adult T cell leukemia (ATL) patients except for very few cases in remission. In the present study, ATL cells were examined for susceptibility to HTLV-I-specific CTL derived from a patient with HAM/TSP. These CTL have been well characterized, and found to be HLA-A2-restricted CD8 positive CTL recognizing HTLV-I Tax. HLA-matched leukemia cells of an ATL patient were efficiently killed by these CTL after an overnight incubation. However, ATL cells immediately after isolation from the peripheral blood were marginally susceptible to the CTL. Addition of synthetic peptide corresponding to the CTL epitope to the assay enabled the CTL to kill the fresh ATL cells, indicating that MHC class I molecules were sufficiently expressed on the leukemia cells. Scarcity of HTLV-I antigens in the fresh ATL cells and induction of these antigens by in vitro incubation were demonstrated both on the cell surface and in the cytoplasm. The levels of HTLV-I tax mRNA were significantly lower in the fresh ATL cells as compared to the cultured ATL cells, whereas the levels of HTLV-I proviral tax gene did not differ among these cells. This suppression of HTLV-I transcription in fresh ATL cells accounts for in vitro resistance to the CTL, and could be a reason for the persistence of HTLV-I infection in vivo. These observations should be taken into consideration in developing immune therapy of ATL.
Keywords: Gene Products, tax/METABOLISM Human HTLV-I/GENETICS/*IMMUNOLOGY HTLV-I Antigens/*ANALYSIS Immunotherapy Leukemia, T-Cell/GENETICS/*IMMUNOLOGY/THERAPY Paraparesis, Tropical Spastic/IMMUNOLOGY T-Lymphocytes, Cytotoxic/IMMUNOLOGY Transcription, Genetic ABSTRACT 940830
M9480795
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Important note: Information in this article was accurate in 1994. The state of the art may have changed since the publication date.
