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International Immunology Advance Access originally published online on May 19, 2008
International Immunology 2008 20(7):893-900; doi:10.1093/intimm/dxn047
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© The Japanese Society for Immunology. 2008. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

In vivo modulation of antigen-experienced cells in response to high-dose oral antigen: deletion but no evidence for alterations in the cytokine phenotype

Friderike Blumenthal-Barby1, Katharina Eulenburg1, Arnhild Schrage2, Martin Zeitz2, Alf Hamann1 and Katja Klugewitz2

1 Experimentelle Rheumatologie, Charité Campus Mitte, Berlin, Germany
2 Medizinische Klinik I, Charité Campus Benjamin Franklin, Hindenburgdamm 30, 12203 Berlin, Germany

Correspondence to: K. Klugewitz; E-mail: katja.klugewitz{at}charite.de

Whether also antigen-experienced CD4+ T cell populations undergo modulations upon oral antigen uptake supporting systemic unresponsiveness is still not fully understood. Using an adoptive transfer model with chicken ovalbumin (OVA)-specific T cells, we demonstrated that absolute numbers of transferred ex vivo-isolated CD4+ memory T cells and in vitro-polarized Th1 cells considerably decrease within spleen and liver upon repetitive OVA feeding. As a consequence, these mice did not mount a delayed-type hypersensitivity reaction after OVA challenge. OVA-specific Th1 cells re-isolated from the liver showed augmented signs of apoptosis. However, there was no evidence that transferred effector or memory T cells acquired a regulatory phenotype, became anergic or underwent immune deviation. Our data suggest that oral antigen application does not induce alterations in the phenotype of CD4+ effector and memory T cells. Instead, deletion of antigen-experienced CD4+ T cells preferentially within the liver might be a major mechanism contributing to antigen-specific systemic unresponsiveness upon oral antigen uptake.

Keywords: CD4+ memory T cells, deletion, oral antigen, Th1 cells

Transmitting editor: A. Radbruch

Received 11 June 2007, accepted 22 April 2008.


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