Drug resistance results in alterations in expression of immune recognition molecules and failure to express Fas (CD95)

It is demonstrated that methotrexate/cisplatin‐sensitive L1210 cells express low levels of major histocompatibility complex (MHC) class II relative to the high levels expressed on methotrexate (MTX)/cisplatin‐resistant L1210/DDP cells. L1210 cells express cell‐surface Fas, while the L1210/DDP cells...

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Bibliographic Details
Published in:Immunology and cell biology 1998-08, Vol.76 (4), p.350-356
Main Authors: Bhushan, A, Kupperman, JL, Stone, JE, Kimberly, PJ, Calman, NS, Hacker, MP, Birge, RB, Tritton, TR, Newell, MK
Format: Article
Language:English
Subjects:
Animals
Antigens, CD - biosynthesis
Antimetabolites, Antineoplastic - pharmacology
Apoptosis
B7-1 Antigen - biosynthesis
B7-2 Antigen
cancer
Carcinogens - pharmacology
Cell Line
Dose-Response Relationship, Drug
Drug Resistance
Fas (CD95)
fas Receptor - biosynthesis
immune recognition
Immune System - drug effects
Kinetics
L1210
Membrane Glycoproteins - biosynthesis
methotrexate
Methotrexate - pharmacology
MHC
Mice
Staurosporine - pharmacology
Trimetrexate - pharmacology
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Summary:It is demonstrated that methotrexate/cisplatin‐sensitive L1210 cells express low levels of major histocompatibility complex (MHC) class II relative to the high levels expressed on methotrexate (MTX)/cisplatin‐resistant L1210/DDP cells. L1210 cells express cell‐surface Fas, while the L1210/DDP cells express no cell‐surface Fas. Expression of costimulatory molecules B7‐1/B7‐2 and Fas is increased on L1210 cells, but not L1210/DDP, in the presence of methotrexate or trimetrexate (TMTX). Therefore, a component of the mechanism of action of some anti‐cancer agents may be to facilitate immune recognition and T cell‐directed, Fas‐induced cell death. Loss of cell‐surface Fas expression and failure of Fas (CD95)‐dependent apoptotic death has been observed when cells develop drug resistance. The defect in apoptosis can be overcome by anti‐cancer agents or experimental manipulation that induce Fas expression on the drug‐resistant cells.
ISSN:0818-9641
1440-1711
DOI:10.1046/j.1440-1711.1998.00758.x