Effects of stress on lysability of tumor targets by cytotoxic T cells and tumor necrosis factor.
The effects of stress on four tumor cell lines are analyzed in view of the possibility that stress protects tumor cells against immune attack. We show that stress causes resistance to CTL and TNF in two cell lines. Induction of resistance is time dependent and reversible and not due to failure of killer cells to interact with stressed targets. It is shown that stress induces stress proteins concomitant with induction of resistance to killer cells and TNF. Moreover experiments are presented suggesting that resistance to either immune effector is due to independent mechanisms. The conclusion that stress can induce mechanisms in targets that interfere with the action of TNF as well as with target lysis following a lethal hit by CTL is discussed.
Department of Microbiology, University of Southern California, Los Angeles 90033.
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S
Sugawara
M
M
Nowicki
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S
Xie
H J
HJ
Song
G
G
Dennert
D000818:Animals; D001384:Azetidines / Q000494:pharmacology; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000502:physiology; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D003602:Cytotoxicity, Immunologic; D003847:Deoxyglucose / Q000494:pharmacology; D006360:Heat-Shock Proteins / Q000096:biosynthesis; D006358:Hot Temperature; D007111:Immunity, Cellular; D066298:In Vitro Techniques; D007295:Inositol Phosphates / Q000378:metabolism; D051379:Mice; D013312:Stress, Physiological / Q000276:immunology*; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000633:toxicity*; D014415:Tunicamycin / Q000494:pharmacology
D001384:Azetidines; D006360:Heat-Shock Proteins; D007295:Inositol Phosphates; D014409:Tumor Necrosis Factor-alpha; D014415:Tunicamycin; D000001:Calcimycin; D003847:Deoxyglucose; D002118:Calcium