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Cited by 316

The DOI matches its Crossref record; 38 of the 38 references it cites were found in a registry or an index.

DC-derived IL-18 drives Treg differentiation, murine Helicobacter pylori–specific immune tolerance, and asthma protection

Open access
Oertli, Mathias, Sundquist, Malin, Hitzler, Iris, Engler, Daniela B., Arnold, Isabelle C., Reuter, Sebastian, Maxeiner, Joachim, Hansson, Malin, Taube, Christian, Quiding-Järbrink, Marianne, Müller, Anne·2012·Journal of Clinical Investigation
DOI 10.1172/jci61029
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Abstract

Persistent colonization with the gastric bacterial pathogen Helicobacter pylori causes gastritis and predisposes infected individuals to gastric cancer. Conversely, it is also linked to protection from allergic, chronic inflammatory, and autoimmune diseases. We demonstrate here that H. pylori inhibits LPS-induced maturation of DCs and reprograms DCs toward a tolerance-promoting phenotype. Our results showed that DCs exposed to H. pylori in vitro or in vivo failed to induce T cell effector functions. Instead, they efficiently induced expression of the forkhead transcription factor FoxP3, the master regulator of Tregs, in naive T cells. Depletion of DCs in mice infected with H. pylori during the neonatal period was sufficient to break H. pylori-specific tolerance. DC depletion resulted in improved control of the infection but also aggravated T cell-driven immunopathology. Consistent with the mouse data, DCs infiltrating the gastric mucosa of human H. pylori carriers exhibited a semimature DC-SIGN(+)HLA-DR(hi)CD80(lo)CD86(lo) phenotype. Mechanistically, the tolerogenic activity of H. pylori-experienced DCs was shown to require IL-18 in vitro and in vivo; DC-derived IL-18 acted directly on T cells to drive their conversion to Tregs. CD4(+)CD25(+) Tregs from infected wild-type mice but not Il18(-/-) or Il18r1(-/-) mice prevented airway inflammation and hyperresponsiveness in an experimental model of asthma. Taken together, our results indicate that tolerogenic reprogramming of DCs ensures the persistence of H. pylori and protects against allergic asthma in a process that requires IL-18.

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Metadata

Authors
Oertli, M., Sundquist, M., Hitzler, I., Engler, D. B., Arnold, I. C., Reuter, S., Maxeiner, J., Hansson, M., Taube, C., Quiding-Järbrink, M., & Müller, A.
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
2012-03-01
Volume
122
Issue
3
Pages
1082-1096
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci61029
OpenAlex
W2123960655
Cited by
316
References
38
FWCI
11.09
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: DC-derived IL-18 drives Treg differentiation, murine Helicobacter pylori–specific immune tolerance, and asthma protection. https://app.cochat.ai/papers/10.1172/jci61029
The paper
Oertli, M., Sundquist, M., Hitzler, I., Engler, D. B., Arnold, I. C., Reuter, S., Maxeiner, J., Hansson, M., Taube, C., Quiding-Järbrink, M., & Müller, A. (2012). DC-derived IL-18 drives Treg differentiation, murine Helicobacter pylori–specific immune tolerance, and asthma protection. Journal of Clinical Investigation. https://doi.org/10.1172/jci61029

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.