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Infection and Immunity, March 2001, p. 1714-1721, Vol. 69, No. 3
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.3.1714-1721.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Adoptive Transfer of CD4+ T Cells Specific for Subunit A of Helicobacter pylori Urease Reduces H. pylori Stomach Colonization in Mice in the Absence of Interleukin-4 (IL-4)/IL-13 Receptor Signaling

Bernadette Lucas, Dirk Bumann, Anna Walduck, Jan Koesling, Leyla Develioglu, Thomas F. Meyer,* and Toni Aebischer

Max-Planck-Institute for Infection Biology, Department of Molecular Biology, Schumannstraße 21/22, 10117 Berlin, Germany

Received 20 September 2000/Returned for modification 6 November 2000/Accepted 18 December 2000

Protection in the murine model of Helicobacter pylori infection may be mediated by CD4+ T cells, but the mechanism remains unclear. To better understand how protection occurs in this model, we generated and characterized H. pylori urease-specific CD4+ T cells from BALB/c mice immunized with Salmonella enterica serovar Typhimurium expressing H. pylori urease (subunits A and B). The CD4+ T cells were found to be specific for subunit A (UreA). Upon antigen-specific stimulation, expression of interleukin 4 (IL-4), IL-10, gamma interferon (IFN-gamma ), and tumor necrosis factor alpha was induced. Immunocytochemical analysis showed that the majority of cells produced IFN-gamma and IL-10. Adoptive transfer of the UreA-specific CD4+ T cells into naive syngeneic recipients led to a threefold reduction in the number of bacteria in the recipient group when compared to that in the nonrecipient group. Stomach colonization was also reduced significantly after transfer of these cells into patently infected mice. Adoptive transfer of UreA-specific CD4+ T cells into IL-4 receptor alpha  chain-deficient BALB/c mice indicated that IL-4 and IL-13 were not critical in the control of bacterial load. In addition, synthetic peptides were used to identify three functional T-cell epitopes present in subunit A which were recognized by the UreA-specific T cells. Analysis of H. pylori-specific cellular immune responses in recipient challenged and nonrecipient infected mice indicated a strong local restriction of the response in infected animals. The implications of these findings for the mechanism of protection and the development of peptide-based vaccination are discussed.

* Corresponding author. Mailing address: Max-Planck-Institute for Infection Biology, Department of Molecular Biology, Schumannstraße 21/22, 10117 Berlin, Germany. Phone: 49 30 28460 400. Fax: 49 30 28460 401. E-mail: meyer{at}mpiib-berlin.mpg.de.

Infection and Immunity, March 2001, p. 1714-1721, Vol. 69, No. 3
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.3.1714-1721.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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