Heat-shocked A20 lymphoma cells fail to induce degranulation of cytotoxic T lymphocytes: Possible mechanism of resistance

A1 Journal article (refereed)


Internal Authors/Editors


Publication Details

List of Authors: Jackson KM, DeLeon M, Sistonen L, Verret CR
Publisher: ACADEMIC PRESS INC
Publication year: 2000
Journal: Cellular Immunology
Journal acronym: CELL IMMUNOL
Volume number: 203
Issue number: 1
Start page: 12
End page: 18
Number of pages: 7
ISSN: 0008-8749


Abstract

A20 lymphoma cells were subjected to heat shock for 2 h at 42 and 43 +/- 0.1 degrees C and then evaluated at 37 degrees C for sensitivity to lysis by intact allo-specific cytotoxic T lymphocytes (CTLs), perforin-containing granules isolated from CTLs, and Fas-mediated apoptosis. Heat shock at 42 degrees C caused little change in sensitivity of the lymphoma cell line to lysis by intact CTLs or their isolated cytotoxic granules, but caused increased sensitivity to Fas-mediated apoptosis. However, A20 cells shocked at 43 degrees C declined significantly in sensitivity to lysis by intact CTLs, while remaining very sensitive to perforin granules and to Fas-mediated apoptosis. Expression of the inducible heat shock protein was observed in A20 cells incubated at 43 degrees C, but not in those incubated at 42 degrees C, suggesting a role for heat shock proteins. Furthermore, A20 cells shocked at 43 degrees C did not provoke degranulation and secretion of granzymes by antigen-specific CTLs, although formation of CTL-target conjugates and levels of MHC class I molecules remained unchanged. These observations demonstrate that hyperthermia or febrile conditions may reduce susceptibility of target cells to CTL attack due to failure of antigen presentation and the inability of CTLs to recognize heat stressed targets, thus enabling targets to escape CTL attack. (C) 2000 Academic Press.


Keywords

apoptosis, heat shock protein 70, perforin, T lymphocytes, tumor cells

Last updated on 2019-15-10 at 02:46