HEAT-SHOCK OF NORMAL T-CELLS AND T-CELL LINES DOWN-REGULATES THE TCR CD3-MEDIATED CYTOPLASMIC CA2+ RESPONSES AND THE PRODUCTION OF INOSITOLTRISPHOSPHATE/

The application of heat shock to different types of cells is known to cause multiple biochemical and metabolic changes. The predominant even t though is an increased synthesis and expression of a family of prote ins, the heat-shock proteins (Hsp). Some of these proteins are current ly considered to be involved in the signal transduction pathway. We in vestigated for any possible effects of heating fresh normal peripheral T-cells and T-cell lines, on the early signal transduction events whi ch follow the antigen (Ag) receptor-complex (TCR/CD3) crosslinking. Mo re specifically, the Ag-receptor-initiated free cytoplasmic Ca2+ ([Ca2 +](i)) responses and the production of inositol 1,4,5-trisphosphate (I P3) were evaluated. Heating fresh unmanipulated peripheral T-cells 8 h ours before the TCR/CD3 stimulation resulted in decreased [Ca2+](i) re sponses. This was also true for cells of normal short-term T-cell line s as well. The TCR/CD3-mediated production of IP3, which is a mediator of the [Ca2+](i) response, was also decreased in heat-shocked T-cells .