help button home button
AJRCCM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by SMITH, K. M.
Right arrow Articles by GARSIDE, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by SMITH, K. M.
Right arrow Articles by GARSIDE, P.

Am. J. Respir. Crit. Care Med., Volume 162, Number 4, October 2000, S175-S178

Oral Tolerance

K. M. SMITH, A. D. EATON, L. M. FINLAYSON, and P. GARSIDE

Department of Immunology and Bacteriology, University of Glasgow, Glasgow, United Kingdom

The intestinal immune system discriminates between potentially harmful and harmless foreign proteins. The basis for this differential response may be related to the conditions of antigen presentation by antigen-presenting cells, as determined by their phenotype or activation state. How these conditions affect specific immunologic unresponsiveness to later challenge with an antigen is not known. Two possible mechanisms are the induction of anergy or deletion of responsive cells and the activation of regulatory cells or mediators, and the mechanism may very depending on the tolerizing regimen used. Should regulatory cells be involved, they are speculated to induce tolerance through their production of inhibitory cytokines, such as IL-4, IL-10, and TGF-beta . Studies using specific antibodies and selective genetic knockout (KO) strains of mice, however, have provided conflicting data. A final intriguing possibility is that tolerance results from cognate interactions between T cells and APCs, so that tolerant T cells or APCs prime T cells they contact to deliver a tolerogenic signal to the next T cell they encounter, possibly through a function dependent on interactions between Notch family receptors and their ligands. As with many questions in mucosal immunology, definition of the mechanisms of oral tolerance (OT) has proved difficult to address experimentally, but promising approaches include study of the distribution of fed antigen, of targeted genetic KOs, and of transgenic strains.




This article has been cited by other articles:


Home page
 JEMHome page
H.-H. Lin, D. E. Faunce, M. Stacey, A. Terajewicz, T. Nakamura, J. Zhang-Hoover, M. Kerley, M. L. Mucenski, S. Gordon, and J. Stein-Streilein
The macrophage F4/80 receptor is required for the induction of antigen-specific efferent regulatory T cells in peripheral tolerance
J. Exp. Med., May 16, 2005; 201(10): 1615 - 1625.
[Abstract] [Full Text] [PDF]

Home page
 JEMHome page
I. Cima, N. Corazza, B. Dick, A. Fuhrer, S. Herren, S. Jakob, E. Ayuni, C. Mueller, and T. Brunner
Intestinal Epithelial Cells Synthesize Glucocorticoids and Regulate T Cell Activation
J. Exp. Med., December 20, 2004; 200(12): 1635 - 1646.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. Rev.Home page
M. F. Lipscomb and B. J. Masten
Dendritic Cells: Immune Regulators in Health and Disease
Physiol Rev, January 1, 2002; 82(1): 97 - 130.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
M. J. TOBIN
Asthma, Airway Biology, and Allergic Rhinitis in AJRCCM 2000
Am. J. Respir. Crit. Care Med., November 1, 2001; 164(9): 1559 - 1580.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Proc. Am. Thorac. Soc. Am. J. Respir. Cell Mol. Biol.
Copyright © 2000 American Thoracic Society 		  The ATS Has Opened Search for New PATS Editor