ACTIVATION SIGNALS REGULATE HEAT-SHOCK TRANSCRIPTION FACTOR-1 IN HUMAN B-LYMPHOCYTES

We previously showed that the ability of human B lymphocytes to elicit a cytoprotective heat shock response when confronted by heat or other stresses was dependent upon the state of cell activation. This was un expected, considering the highly conserved nature of the heat shock re sponse and the widely held belief that all nonmutated mature cells wer e capable of eliciting a heat shock response when stressed. To elucida te the mechanism by which activation primes B cells to respond to stre sses, we examined heat shock transcription factor 1 (hHSF1) in B cells since this factor appears to be solely responsible for stress-induced transcription of heal shock genes in human cells. In the current repo rt, we show that hHSF1-DNA binding complexes are undetectable in extra cts of unactivated B cells. In fact, hHSF1 protein is not constitutive ly expressed in unactivated B cells, nor is its synthesis stress-induc ible. However, following activation, hHSF1 can be found in either a tr anscriptionally active or an inactive state, depending upon whether th e cell has been stressed or not. Thus, activation pathways play an imp ortant role in enabling B cells to survive and function properly in th e context of physiologic stresses by regulating hHSF1. (C) 1997 Wiley- Liss, Inc.