You are currently viewing the summary.
View Full TextLog in to view the full text
AAAS login provides access to Science for AAAS members, and access to other journals in the Science family to users who have purchased individual subscriptions.
More options
Download and print this article for your personal scholarly, research, and educational use.
Buy a single issue of Science for just $15 USD.
Summary
The gut poses a unique challenge to the organism. The host must tolerate beneficial commensal bacteria, yet allow for rapid protective responses to invading pathogens. Failure to maintain this balance may cause intestinal disorders such as chronic inflammatory bowel disease. Fortunately, a dynamic, yet robust, state of chronic, low-grade inflammation maintains this balance (“primed homeostasis”). Thus, the host actively engages the gut microbiota, controlling its composition by secreting antimicrobial peptides and immunoglobulins. Conversely, commensals shape the gut-associated immune system by controlling the prevalence of distinct T cell populations (1). On page 1477 of this issue, Mortha et al. (2) show how communication between specific myeloid and lymphoid cells controls immune homeostasis under exposure to the gut microflora. Such cellular details of this steady state may guide the development of rational therapies for intestinal inflammatory conditions.