Showing papers by "Torben Plesner published in 1990"

Transmembrane Signalling via HLA-DR Molecules on T Cells from a Sezary T-Cell Leukaemia Line

Abstract: The human Sezary T-cell leukaemia line, HUT78, represents a population of activated T cells, ie they are HLA-DR+ and IL-2R+ We have analysed the capacity of HUT78 cells (1) to stimulate HLA-DR-specific T-cell lines or clones and (2) to be induced to synthesize IL-2 by anti-HLA-DR monoclonal antibodies The results of our experiments show that HLA-DR molecules on HUT78 cells can stimulate at least one HLA-DR-specific T-cell clone and can act as transmembrane signal transmitters

T-cell activation. III. Attempts to activate MHC class I-negative and class I-transfected EL4 T-lymphoma cells by immobilized anti-CD3 antibody.

Abstract: The aim of this study was to examine whether the unresponsiveness of MHC class I-negative subclones of the EL-4 thymoma lo CD3 cross-linking can be restored by transfection of class I genes into the H-2-negative cells. Cell activation experiments with selected MHC class I-negative subclones and H-2b-and H-2Ld-positive transfectants showed that these cells are equally capable of secreting interleukin 2 (IL-2) after exposure to the phorbol ester phorbol 12-mvristalc 13-acetale (PMA) and ionomycin. In contrast, only the parental H-2-positive EL4 cells are capable of responding to treatment with immobilized anti-CD3 antibody with IL-2 secretion and IL-2 receptor expression. Measurements of intracellular free Ca2+ (Ca2+i) following anti-CD3 antibody-induced cross-linking of parental EL4 cells and H-2-negativeand H-2b gene-transfected subclones showed that the parental cells and two of the class I transfectants, one H-2-positiveand one H-2-negative. responded with a slow rise in Ca2+,. whereas one H-2-positive transfected cell clone was completely refractory to CD3 cross-linking. Modulation experiments using parental EL 4 cells, H-2-negative subclones and H-2-positive transfectants demonstrated that the CD3 and class I molecules of these different cells are modulated to the same extent after exposure lo specific antibodies. The present findings thus indicate that the unresponsiveness of H-2-negative EL4 subclone cells not CD3 cross-linking is not functionally associated with a lack of class I surface expression.