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Cited by 32

The DOI matches its Crossref record; 61 of the 61 references it cites were found in a registry or an index.

Infection of Myeloid Dendritic Cells with Listeria monocytogenes Leads to the Suppression of T Cell Function by Multiple Inhibitory Mechanisms

Popov, Alexey, Driesen, Julia, Abdullah, Zeinab, Wickenhauser, Claudia, Beyer, Marc, Debey-Pascher, Svenja, Saric, Tomo, Kummer, Silke, Takikawa, Osamu, Domann, Eugen, Chakraborty, Trinad, Krönke, Martin, Utermöhlen, Olaf, Schultze, Joachim L·2008·The Journal of Immunology
DOI 10.4049/jimmunol.181.7.4976
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Abstract

Myeloid dendritic cells (DC) and macrophages play an important role in pathogen sensing and antimicrobial defense. In this study we provide evidence that myeloid DC respond to infection with Listeria monocytogenes with simultaneous induction of multiple stimulatory and inhibitory molecules. However, the overall impact of infected DC during T cell encounter results in suppression of T cell activation, indicating that inhibitory pathways functionally predominate. Inhibitory activity of infected DC is effected mainly by IL-10 and cyclooxygenase 2-mediated mechanisms, with soluble CD25 acting as an IL-2 scavenger as well as by the products of tryptophan catabolism. These inhibitory pathways are strictly TNF-dependent. In addition to direct infection, DC bearing this regulatory phenotype can be induced in vitro by a combination of signals including TNF, TLR2, and prostaglandin receptor ligation and by supernatants derived from the infected cells. Both infection-associated DC and other in vitro-induced regulatory DC are characterized by increased resistance to infection and enhanced bactericidal activity. Furthermore, myeloid DC expressing multiple regulatory molecules are identified in vivo in granuloma during listeriosis and tuberculosis. Based on the in vivo findings and the study of in vitro models, we propose that in granulomatous infections regulatory DC may possess dual function evolved to protect the host from disseminating infection via inhibition of granuloma destruction by T cells and control of pathogen spreading.

Overview

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Crossref · 10.4049/jimmunol.181.7.4976

Cites

61 of 61 references verified0 citation errors · 0 not checkable

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Metadata

Authors
Popov, A., Driesen, J., Abdullah, Z., Wickenhauser, C., Beyer, M., Debey-Pascher, S., Saric, T., Kummer, S., Takikawa, O., Domann, E., Chakraborty, T., Krönke, M., Utermöhlen, O., & Schultze, J. L.
Affiliations
  • Genomics and Immunoregulation, Institute for Life and Medical Sciences, University of Bonn , Bonn,
  • Institute for Medical Microbiology, Immunology and Hygiene
  • Institute for Pathology
  • Institute for Neurophysiology, University of Cologne , Cologne,
  • National Institute for Longevity Sciences, National Center for Geriatrics and Gerontology , Obu, Aichi,
  • Institute of Medical Microbiology, University of Giessen , Giessen,
Venue
The Journal of Immunology
Publisher
Oxford University Press (OUP)
Published
2008-10-01
Volume
181
Issue
7
Pages
4976-4988
ISSN
  • 1550-6606
  • 0022-1767
DOI
10.4049/jimmunol.181.7.4976
Cited by
32
References
61
Language
en
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)

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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

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Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

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.