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BACKGROUND:

Control of the inflammatory response is critical to maintaining homeostasis, and failure to do so contributes to the burden of chronic inflammation associated with several disease states. The mechanisms that underlie immunosuppression, however, remain largely unknown. While defects in autophagy machinery have been associated with inflammatory pathologies, we now appreciate that autophagic components participate in non-canonical pathways distinct from classical autophagy. We have previously demonstrated that LC3-associated phagocytosis (LAP), a non-canonical autophagic process dependent on Rubicon (RUBCN), contributes to immunosuppression.

OBJECTIVE:

We used Rubcn−/− mice to examine the role of in mediating the UV-induced immunotolerant program in a model of contact hypersensitivity (CHS).

METHODS:

Flow cytometry and transcriptional analysis was used to measure …