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Infection and Immunity, March 2001, p. 1714-1721, Vol. 69, No. 3
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-
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
), and tumor necrosis factor alpha was
induced. Immunocytochemical analysis showed that the majority of cells
produced IFN-
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
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.
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