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Inflammation & Allergy-Drug Targets
(Formerly Current Drug Targets - Inflammation & Allergy)
ISSN (Print): 1871-5281
ISSN (Online): 2212-4055
VOLUME: 5
ISSUE: 3
DOI: 10.2174/187152806778256034      Price:  $58









Oral Tolerance and TGF-β -Producing Cells

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Author(s): Ana M. C. Faria and Howard L. Weiner
Pages 179-190 (12)
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.
Keywords:
Oral tolerance, TGF-, Th3 cells, LAP+ cells, regulatory T cells
Affiliation:
Center for Neurologic Diseases,Brigham and Women's Hospital, Harvard Medical School, 221 Longwood Ave, Boston, MA 02115, USA.