Increased class Ib antigen display on TAP-2 mutant cells by a mitochondrial function inhibitor

• Published in: Cellular immunology 1997-07, Vol.179 (1), p.10-15
• Main Authors: Hermel, E, Grigorenko, E, Aldrich, C J
• Format: Article
• Language: English
• Subjects: Adenosine Triphosphatases - antagonists & inhibitors; Animals; Antigen Presentation - genetics; Antigen Presentation - immunology; ATP-Binding Cassette Transporters - genetics; ATP-Binding Cassette Transporters - immunology; ATP-Binding Cassette, Sub-Family B, Member 3; Carbonyl Cyanide m-Chlorophenyl Hydrazone - pharmacology; Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone - pharmacology; Cell Line; Dicyclohexylcarbodiimide - pharmacology; Enzyme Inhibitors - pharmacology; Histocompatibility Antigens Class I - immunology; Mice; Mice, Inbred BALB C; Mice, Inbred C3H; Mice, Inbred C57BL; Mitochondria - drug effects; Mitochondria - physiology; Mutation; Oligomycins - pharmacology; Peptides - immunology; T-Lymphocytes - immunology; T-Lymphocytes, Cytotoxic - immunology; Uncoupling Agents - pharmacology
• ISSN: 0008-8749
• DOI: 10.1006/cimm.1997.1145

Class I histocompatibility antigen display is defective in the RMA-S mutant cell line due to a mutation in the Tap-2 gene, which encodes a peptide transporter. Incubation of RMA-S cells with oligomycin, an inhibitor of mitochondrial ATPase, strongly increased lysis by cytotoxic T lymphocytes (CTL) specific for the class Ib antigen H2-M3, and lysis by Qa-1b-specific CTL was restored. Oligomycin did not affect normal class I display on RMA cells. Treatment of RMA-S cells with other inhibitors of mitochondrial function failed to increase lysis by anti-H2-M3 or Qa-1b CTL. Lysis by allogenic CTL specific for H-2b antigens was either not enhanced or only weakly increased, depending upon the H-2 haplotype of the alloreactive effector cells used.