Autophagy, viruses, and intestinal immunity

To highlight recent findings that identify an essential role for the cellular degradative pathway of autophagy in governing a balanced response to intestinal pathogens and commensals.

Following the genetic association of autophagy with inflammatory bowel disease susceptibility, increasing evidence indicates that this pathway functions in various epithelial lineages to support the intestinal barrier. New studies are also revealing that autophagy proteins dictate the quality and magnitude of immune responses. Mouse models, in particular, suggest that autophagy and inflammatory bowel disease susceptibility genes regulate inflammatory responses to viruses, a finding that coincides with an increasing appreciation that viruses have intricate interactions with the host and the microbiota beyond the obvious host-pathogen relationship.

Autophagy and other immunological or stress response pathways intersect in mucosal immunity to dictate the response to pathogenic and commensal agents. The development of novel treatment strategies, as well as prognostic and diagnostic tools for gastrointestinal disorders, will be greatly facilitated by a deeper understanding of these interactions at the cell type and microbe-specific manner, which includes less appreciated components of the microbiota, such as eukaryotic and prokaryotic viruses.