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Inflammation & Allergy - Drug Targets (Discontinued)


ISSN (Print): 1871-5281
ISSN (Online): 2212-4055

Oral Tolerance and TGF-β -Producing Cells

Author(s): Ana M. C. Faria and Howard L. Weiner

Volume 5, Issue 3, 2006

Page: [179 - 190] Pages: 12

DOI: 10.2174/187152806778256034

Price: $65


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-β plays a central role in oral tolerance as a mediator secreted by Th3 cells. In addition, recent pieces of evidence suggest that TGF-β 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-β . A membrane-bound form of TGF-β (containing latency-associated peptide - LAP) has also been described and LAP+ CD4+ T cells mediate suppression in the gut by a TGF- -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-β production by either macrophages that phagocyte apoptotic cells or by the dying T cells. Thus, it appears that TGF-β -producing cells are not only crucial for oral tolerance, but they may be master regulators of most of the mechanisms triggered by antigen feeding.

Keywords: Oral tolerance, TGF-, Th3 cells, LAP+ cells, regulatory T cells

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