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Cited by 160

The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.

Autocrine IL-10 Induces Hallmarks of Alternative Activation in Macrophages and Suppresses Antituberculosis Effector Mechanisms without Compromising T Cell Immunity

Open access
Schreiber, Tanja, Ehlers, Stefan, Heitmann, Lisa, Rausch, Alexandra, Mages, Jörg, Murray, Peter J, Lang, Roland, Hölscher, Christoph·2009·The Journal of Immunology

Abstract

Elevated IL-10 has been implicated in reactivation tuberculosis (TB). Since macrophages rather than T cells were reported to be the major source of IL-10 in TB, we analyzed the consequences of a macrophage-specific overexpression of IL-10 in transgenic mice (macIL-10-transgenic) after aerosol infection with Mycobacterium tuberculosis (Mtb). MacIL-10 transgenic mice were more susceptible to chronic Mtb infection than nontransgenic littermates, exhibiting higher bacterial loads in the lung after 12 wk of infection and dying significantly earlier than controls. The differentiation, recruitment, and activation of Th1 cells as well as the induction of IFN-γ-dependent effector genes against Mtb were not affected by macrophage-derived IL-10. However, microarray analysis of pulmonary gene expression revealed patterns characteristic of alternative macrophage activation that were overrepresented in Mtb-infected macIL-10 transgenic mice. Importantly, arginase-1 gene expression and activity were strikingly enhanced in transgenic mice accompanied by a reduced production of reactive nitrogen intermediates. Moreover, IL-10-dependent arginase-1 induction diminished antimycobacterial effector mechanisms in macrophages. Taken together, macrophage-derived IL-10 triggers aspects of alternative macrophage activation and promotes Mtb recrudescence independent of overt effects on anti-TB T cell immunity.

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Metadata

Authors
Schreiber, T., Ehlers, S., Heitmann, L., Rausch, A., Mages, J., Murray, P. J., Lang, R., & Hölscher, C.
Venue
The Journal of Immunology
Published
2009-07
Volume
183
Issue
2
Pages
1301-1312
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
OpenAlex
W1581627029
Cited by
160
References
9
FWCI
10.26
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Autocrine IL-10 Induces Hallmarks of Alternative Activation in Macrophages and Suppresses Antituberculosis Effector Mechanisms without Compromising T Cell Immunity. https://app.cochat.ai/papers/10.4049/jimmunol.0803567
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Schreiber, T., Ehlers, S., Heitmann, L., Rausch, A., Mages, J., Murray, P. J., Lang, R., & Hölscher, C. (2009). Autocrine IL-10 Induces Hallmarks of Alternative Activation in Macrophages and Suppresses Antituberculosis Effector Mechanisms without Compromising T Cell Immunity. The Journal of Immunology. https://doi.org/10.4049/jimmunol.0803567

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

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