Development of spontaneous uterine tumors in low molecular mass polypeptide-2 knockout mice.
The presentation of antigenic peptides by MHC class I molecules is important for tumor rejection by CTLs. Such antigenic peptides are generated as a result of the degradation of intracellular proteins by the proteasome pathway, a process that is influenced by the IFN-gamma-inducible low molecular mass polypeptide-2 (LMP2) subunit of the proteasome complex. LMP2 knockout mice thus exhibit a defect in proteasome function. Female LMP2(-/-) mice are now shown to develop uterine neoplasms, with a disease prevalence of approximately 36% by 12 months of age. This observation indicates that proteasome function is essential for MHC class I-mediated tumor rejection by CTLs.
Hayashi
Takuma
T
Immunobiology Laboratory, Massachusetts General Hospital-East, and Harvard Medical School, Charlestown, Massachusetts 02129, USA.
Faustman
Denise L
DL
D000818:Animals; D003546:Cysteine Endopeptidases; D005260:Female; D015395:Histocompatibility Antigens Class I / Q000276:immunology; D007157:Immunologic Surveillance / Q000235:genetics / Q000276:immunology; D007371:Interferon-gamma / Q000494:pharmacology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008819:Mice, Nude; D014176:Protein Biosynthesis; D011506:Proteins / Q000235:genetics* / Q000276:immunology*; D014594:Uterine Neoplasms / Q000235:genetics* / Q000276:immunology*
D015395:Histocompatibility Antigens Class I; D011506:Proteins; C071313:LMP-2 protein; D007371:Interferon-gamma; D003546:Cysteine Endopeptidases