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

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 II gene promoter, is responsible for lack of MHC class II on most of the MHC class II-negative melanoma cell lines.

We rescued CIITA and MHC class II expression in melanoma cell lines by stable transformation with a CIITA expression vector and assayed for MHC class II-mediated apoptosis.

Reconstitution of CIITA in multiple CIITA-negative melanoma lines restores the apoptotic function of melanoma MHC class II.

Lack of MHC class II 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.