Heat-shock of normal t-cells and T-cell lines downregulates the TCR/CD3-mediated cytoplasmic Ca2+ responses and the production of inositol trisphosphate.

Abstract:

:The application of heat shock to different types of cells is known to cause multiple biochemical and metabolic changes. The predominant event though is an increased synthesis and expression of a family of proteins, the heat-shock proteins (Hsp). Some of these proteins are currently considered to be involved in the signal transduction pathway. We investigated for any possible effects of heating fresh normal peripheral T-cells and T-cell lines, on the early signal transduction events which follow the antigen (Ag) receptor-complex (TCR/CD3) crosslinking. More specifically, the Ag-receptor-initiated free cytoplasmic Ca2+ ([Ca2+]i) responses and the production of inositol 1,4,5-trisphosphate (IP3) were evaluated. Heating fresh unmanipulated peripheral T-cells 8 hours before the TCR/CD3 stimulation resulted in decreased [Ca2+]i responses. This was also true for cells of normal short-term T-cell lines 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.

authors

Liossis SN,Tsokos GC

doi

10.3109/08923979709007672

subject

Has Abstract

pub_date

1997-11-01 00:00:00

pages

511-21

issue

4

eissn

0892-3973

issn

1532-2513

journal_volume

19

pub_type

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