Oral Tolerance and TGF-β -Producing Cells

Title: Oral Tolerance and TGF-β -Producing Cells

Volume: 5 Issue: 3

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

Affiliation:

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

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-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.

Cite this article as:

C. Faria M. Ana and Weiner L. Howard, Oral Tolerance and TGF-β -Producing Cells, Inflammation & Allergy - Drug Targets (Discontinued) 2006; 5 (3) . https://dx.doi.org/10.2174/187152806778256034