CIITA transformation rescues the apoptotic function of MHC class II in melanoma cells

Background: Cell-surface major histocompatibility (MHC) class II molecules contribute to a molecular, intercellular complex that stimulates T-cells. MHC class II molecules also activate signaling pathways leading to apoptosis. Lack of CIITA, a co-activator of the MHC class H gene promoter, is responsible for lack of MHC class H on most of the MHC class II-negative melanoma cell lines. Materials and Methods: We rescued CIITA and MHC class II expression in melanoma cell lines by stable transformation with a CHTA expression vector and assayed for MHC class II-mediated apoptosis. Results: Reconstitution of CIITA in multiple CIITA-negative melanoma lines restores the apoptotic function of melanoma MHC class H. Conclusion: Lack of MHC class 11 transcription, rather than defects in MHC class II protein function or defects in the other components of the MHC class II-stimulated apoptotic pathway, prevents MHC class II-mediated apoptosis in melanoma cells.