Trends in Immunology
Research UpdateMucosal antigen presentation and the control of tolerance and immunity
Section snippets
Dendritic cells control tolerance and immunity at mucosal surfaces
Much prior work has focused on whether unique types of antigen-presenting cells (APCs) function at mucosal surfaces. For example, it has long been recognized that intestinal epithelial cells, particularly specialized enterocytes called M cells, deliver luminal antigens to the mucosal immune system (L. Mayer, New York, NY, USA; M. Neutra, Boston, MA, USA). Although enterocytes express MHC class I and, in some instances, MHC class II, other work has shown that enterocytes do not serve as APCs for
Mucosal surfaces: a unique microenvironment for antigen presentation
How do DCs regulate tolerance and immunity at mucosal surfaces? The cell biology of DCs suggests that the conditions and timing of DC maturation plays an important role (I. Mellman, New Haven, CT, USA). In keeping with the anti-inflammatory environment required in the GALT in the face of constant antigenic challenge, DC subsets within mucosal tissues have unique immune-inductive capabilities (B. Kelsall, Bethesda, MD, USA). Myeloid-lineage-derived DCs in the Peyer's patch are particularly
Regulatory/suppressor T cells are generated in the GALT microenvironment
The once-reviled suppressor T cell has made a dramatic comeback. Subsets of regulatory or suppressor T cells secreting either transforming growth factor β [TGF-β; T helper 3 (Th3) cells; H. Weiner, Boston, MA, USA] or IL-10 (Tr1 cells; M. Roncarolo, Milan, Italy) have been shown to play important roles in both immune suppression and the maintenance of immune homeostasis in the potentially inflammatory gut microenvironment. Functionally nonresponsive ‘anergic’ T cells retain the ability to
Concluding remarks
While highlighting the unique aspects of antigen presentation at mucosal surfaces, this meeting suggested many avenues for future research, particularly with regard to the derivation and function of regulatory T cells.
Acknowledgments
The authors were the program organizers for the meeting, which was sponsored by the Center for the Study of Inflammatory Bowel Disease at Massachusetts General Hospital, Boston, MA, USA. Additional support was provided through unrestricted educational grants from Amgen Inc., Biogen Inc., Celgene Corp. and Immunex Corp.
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