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

A1 Originalartikel i en vetenskaplig tidskrift (referentgranskad)

Interna författare/redaktörer

Publikationens författare: Jackson KM, DeLeon M, Sistonen L, Verret CR
Publiceringsår: 2000
Tidskrift: Cellular Immunology
Tidskriftsakronym: CELL IMMUNOL
Volym: 203
Nummer: 1
Artikelns första sida, sidnummer: 12
Artikelns sista sida, sidnummer: 18
Antal sidor: 7
ISSN: 0008-8749


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.


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

Senast uppdaterad 2020-11-08 vid 03:32