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Published on: November 28, 2010
Development of spontaneous uterine tumors in low molecular mass polypeptide-2 knockout mice
Takuma Hayashi1, Denise L Faustman
1Immunobiology Laboratory, Massachusetts General Hospital-East, and Harvard Medical School, Charlestown, Massachusetts 02129, USA.
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.
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.
