Abstract

Two autologous T cell lines infected with HTLV I are described. T cells from a patient with malignant melanoma were infected with HTLV I by co-culture with a HTLV I-producing T cell line,SLB I. Both T cell lines express identical phenotype (CD3+, CD4+, 4B4+, 2H4−) but they demonstrate marked differences in growth characteristics and function. One of these two lines, referred to as TFTx, established from the autologous tumor activated peripheral blood lymphocytes (PBL), grows in culture without any exogenous interleukin-2 (IL-2), secretes no detectable amount of IL-2 or gamma interferon (IFN) or tumor necrosis factor (TNF) alpha or beta. The other line (TFATx), established from a co-culture between the autologous PBL, lethally irradiated TFTx and the autologous melanoma cells TFM, is IL-2-dependent for growth, secrets IFN gamma and TNF alpha and beta. TFTx exerts profound suppression of generation of cytotoxicity in the autologous PBL in co-culture with the autologous melanoma cells TF-M. In contrast, the TFATx enhances the cytotoxic response in similar co-culture. In addition to suppression of cytotoxic response, supernatant from TFTx suppresses the lectin-activated proliferation of PBL. In 4-h chromium release microcytotoxicity assays, neither line exhibits conventional characteristics of cytotoxic cells. Thus, phenotypically identical HTLV I-infected CD4+ T cell lines derived from the same individual exhibit opposite regulatory functions.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.