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Oral tolerance induction by mucosal administration of cholera toxin B-coupled antigen involves T-cell proliferation in vivo and is not affected by depletion of CD25+ T cells.

Journal article
Authors Annie George-Chandy
Susanne Hultkrantz
Sukanya Raghavan
Cecil Czerkinsky
Michael Lebens
Esbjörn Telemo
Jan Holmgren
Published in Immunology
Volume 118
Issue 3
Pages 311-20
ISSN 0019-2805
Publication year 2006
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Institute of Biomedicine, Department of Microbiology and Immunology
Pages 311-20
Language en
Links dx.doi.org/10.1111/j.1365-2567.2006...
Keywords Administration, Oral, Adoptive Transfer, Animals, CD4-Positive T-Lymphocytes, immunology, Cell Proliferation, Cholera Toxin, immunology, Down-Regulation, immunology, Hemagglutinins, Viral, immunology, Immune Tolerance, immunology, Immunity, Mucosal, Integrins, metabolism, L-Selectin, metabolism, Lymph Nodes, immunology, Lymphocyte Activation, immunology, Male, Mice, Mice, Inbred BALB C, Mice, Transgenic, Receptors, Interleukin-2, analysis, Spleen, immunology, T-Lymphocyte Subsets, immunology, Up-Regulation, immunology
Subject categories Immunology in the medical area

Abstract

Oral administration of antigens coupled to the B subunit of the cholera toxin (CTB) can dramatically reduce the amount of antigen needed for tolerance induction and has been used in several animal models to suppress conditions where the immune system overreacts to foreign and self-antigens. In this study, the cellular events following oral administration of CTB-coupled antigen was investigated. As a model system, limited numbers of CSFE-labelled cells from influenza haemagglutinin peptide (HApep) T-cell transgenic mice were transferred to wild type mice and the mice were then given CTB-coupled HApep orally. The inductive events of CTB-induced tolerance was characterized by extensive proliferation of HApep-specific T cells in the mesenteric lymph nodes (MLNs) and in the spleen. The proliferating cells up-regulated the gut homing molecule alpha4beta7 and down-regulated the high endothelial venule binding molecule L-selectin. Addition of the whole cholera toxin (CT) to CTB-HApep showed a similar pattern as CTB-HApep feeding, with antigen-specific proliferation in the MLN and spleen and expression of alpha4beta7 on the proliferating cells. However, addition of CT to CTB-HApep, produced a stronger and faster proliferative response and abrogated CTB-HA mediated oral tolerance. Feeding of CTB-HApep expanded CD25+ cells in the MLNs. CTB-induced oral tolerance could, however, not be explained by CD25+ dependent regulatory activity, as oral administration of CTB-HApep to mice depleted of CD25+ cells still gave rise to systemic tolerance. Thus, several mechanisms might co-orchestrate the systemic tolerance seen in response to feeding with CTB-coupled antigen.

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