Microbiota: Host Interactions in Mucosal Homeostasis and Systemic Autoimmunity

  1. Dan R. Littman1,3
  1. 1The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, New York 10016
  2. 2The Jill Roberts Center for Inflammatory Bowel Disease, Department of Medicine, Weill-Cornell Medical College, New York, New York 10021
  3. 3Howard Hughes Medical Institute, New York University School of Medicine, New York, New York 10016
  1. Correspondence: dan.littman{at}med.nyu.edu

Abstract

The vertebrate intestinal tract is colonized by hundreds of species of bacteria that must be compartmentalized and tolerated to prevent invasive growth and harmful inflammatory responses. Signaling initiated by commensal bacteria shapes antigen-specific mucosal and systemic adaptive immunity. A distinct type of effector CD4+ T cells, Th17 cells, have a key role in coordinating the inflammatory immune responses that afford protection to pathogens at the mucosal interface. Balancing this powerful inflammatory response, regulatory T cells limit collateral damage and provide antigen-specific tolerance to both food and microbial antigens. Here, we discuss the implications for how the microbiota as a whole contributes to compartmentalization from the host and how individual constituents of the microbiota influence the functions and repertoire of effector T cells and organ-specific autoimmune disease.

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