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- Title
Oral tolerance and TGF-beta-producing cells.
- Authors
Faria, Ana M C; Weiner, Howard L
- Abstract
Multiple mechanisms have been proposed to explain the immune hyporesponsiveness to fed antigens, a phenomenon named oral tolerance. Low doses of orally administered antigen are reported to favor active suppression with the generation of regulatory cells, whereas high doses would favor clonal anergy/deletion. A major conceptual advance in oral tolerance has been the demonstration that TGF-beta plays a central role in oral tolerance as a mediator secreted by Th3 cells. In addition, recent pieces of evidence suggest that TGF-beta may be a primary link between distinct populations of regulatory T cells that are induced by feeding. Conversion of CD4+CD25- into CD4+CD25+ T cells by the expression of FoxP3 involves TGF-beta. A membrane-bound form of TGF-beta (containing latency-associated peptide - LAP) has also been described and LAP+ CD4+ T cells mediate suppression in the gut by a TGF-beta-dependent mechanism. Most of these regulatory T cells are anergic cells indicating that anergy may be also related to Treg induction. Moreover, deletional events taking place in the gut mucosa induce TGF-beta production by either macrophages that phagocyte apoptotic cells or by the dying T cells. Thus, it appears that TGF-beta-producing cells are not only crucial for oral tolerance, but they may be master regulators of most of the mechanisms triggered by antigen feeding.
- Publication
Inflammation & allergy drug targets, 2006, Vol 5, Issue 3, p179
- ISSN
1871-5281
- Publication type
Journal Article
- DOI
10.2174/187152806778256034