Document Detail


Pathogenic T cells persist after reversal of autoimmune disease by immunosuppression with regulatory T cells.
MedLine Citation:
PMID:  23420509     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Autoimmune disease can be prevented with immunosuppressive agents; however, the effectiveness of these treatments in advanced stage of disease and the fate of pathogenic T cells following such treatments are not clear. In this study we demonstrate that a single dose of in vitro-induced Treg cells (iTreg cells) resulted in the functional repair and restitution of stomach tissue that had been severely damaged in advanced autoimmune gastritis. iTreg cells caused depletion or inactivation of autoreactive naïve T cells that were antigen inexperienced, however, autoreactive effector/memory T cells persisted in treated mice, resulting in residual cellular infiltrates within the repaired stomach tissue. The persisting autoreactive T cells were able to rapidly cause autoimmune disease if iTreg cells were removed. Similar data were obtained from mice treated continuously with corticosteroid, in that there was substantial restitution of the gastric mucosa; however, effector T cells persisted and rapidly caused pathology following drug removal. Therefore, iTreg cells or corticosteroid can suppress pathogenic autoreactive cells in advanced autoimmune disease, reversing tissue damage and improving tissue function. However, the persistence of pathogenic T cells represents a disease risk.
Authors:
Eric Tu; Dorothée Bourges; Paul A Gleeson; Desmond K Y Ang; Ian R van Driel
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2013-03-25
Journal Detail:
Title:  European journal of immunology     Volume:  43     ISSN:  1521-4141     ISO Abbreviation:  Eur. J. Immunol.     Publication Date:  2013 May 
Date Detail:
Created Date:  2013-04-25     Completed Date:  2013-06-17     Revised Date:  2013-10-29    
Medline Journal Info:
Nlm Unique ID:  1273201     Medline TA:  Eur J Immunol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  1286-96     Citation Subset:  IM    
Copyright Information:
© 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
Affiliation:
Department of Biochemistry and Molecular Biology, Bio21 Molecular Science and Biotechnology Institute, The University of Melbourne, Parkville, Victoria, Australia.
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MeSH Terms
Descriptor/Qualifier:
Adoptive Transfer
Adrenal Cortex Hormones / pharmacology
Animals
Autoimmune Diseases / immunology,  pathology*,  therapy
Cell Communication
Disease Models, Animal
Gastritis / immunology,  pathology*,  therapy
Immunosuppression
Immunotherapy, Adoptive*
Lymphocyte Activation
Mice
Prednisolone / pharmacology
T-Lymphocytes, Cytotoxic / drug effects,  immunology,  pathology*
T-Lymphocytes, Regulatory / cytology,  immunology*,  transplantation
Chemical
Reg. No./Substance:
0/Adrenal Cortex Hormones; 50-24-8/Prednisolone

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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