It takes guts for tolerance: The phenomenon of oral tolerance and the regulation of autoimmune response


Autoria(s): PERON, Jean Pierre Schatzmann; OLIVEIRA, Ana Paula Ligeiro de; RIZZO, Luiz Vicente
Contribuinte(s)

UNIVERSIDADE DE SÃO PAULO

Data(s)

20/10/2012

20/10/2012

2009

Resumo

The intestinal tract is a peculiar environment due to its constant contact with the microbiota agents, food antigens and other molecules. Such exposure requires the establishment of important regulatory mechanisms in order to avoid inflammatory response and self aggression. In this context, the GALT plays a very relevant role due to the presence of several different cellular populations which are the main players in this phenomenon. Moreover, it was described a while ago that the oral ingestion of a given molecule is able to induce systemic tolerance to the same molecule when it is used as an immunogen by parenteral route, known as oral tolerance. This observation led researches to use these mechanisms to induce tolerance against cognate antigens of different autoimmune diseases. In this context, in this review we focused on several tolerance inducing mechanisms which are relevant not only for the maintenance of intestinal tract but also for the suppression of T effector cells, such as Th1, Th2 and the newly described Th17 cells. To name a few, CD103(+) dendritic cells, Tr1 cells derived IL-10 secretion, Foxp3 conversion and CD4(+)LAP(+) regulatory cells induction are among the recently described features of the tolerogenic environment of the intestinal tract. (C) 2009 Elsevier B.V. All rights reserved.

Identificador

AUTOIMMUNITY REVIEWS, v.9, n.1, p.1-4, 2009

1568-9972

http://producao.usp.br/handle/BDPI/28291

10.1016/j.autrev.2009.02.024

http://dx.doi.org/10.1016/j.autrev.2009.02.024

Idioma(s)

eng

Publicador

ELSEVIER SCIENCE BV

Relação

Autoimmunity Reviews

Direitos

restrictedAccess

Copyright ELSEVIER SCIENCE BV

Palavras-Chave #Oral tolerance #Tolerance #Tregs #Th17 #ROR-GAMMA-T #DENDRITIC CELLS #MUCOSAL TOLERANCE #RETINOIC-ACID #ENCEPHALOMYELITIS #DIFFERENTIATION #INDUCTION #BETA #INTERLEUKIN-10 #INFLAMMATION #Immunology
Tipo

article

original article

publishedVersion