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 accessAbstract
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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Citations
Cites
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“Despite the presence of macrophage-derived IL-10 in the lungs of infected transgenic mice, Th1 cells efficiently expressed effector functions and secreted sufficient IFN- to induce a classical macrophage activation characterized by expression of NOS2 and LRG-47.”
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BackgroundInfluentialSelf-citationThe role of IL-10 in promoting disease progression in Leishmaniasis
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Understanding and exploiting the endogenous interleukin-10/STAT3-mediated anti-inflammatory response
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Cited by
Sabat, R., Grütz, G., Warszawska, K., Kirsch, S., Witte, E., Wolk, K., & Geginat, J. (2010) · Cytokine & Growth Factor Reviews · doi:10.1016/j.cytogfr.2010.09.002 · Cited by 977
The role of IL-10 in immune regulation during M. tuberculosis infection
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Self-citationHalstead, S. B., Mahalingam, S., Marovich, M. A., Ubol, S., & Mosser, D. M. (2010) · The Lancet Infectious Diseases · doi:10.1016/s1473-3099(10)70166-3 · Cited by 409
Mattila, J. T., Ojo, O. O., Kepka-Lenhart, D., Marino, S., Kim, J. H., Eum, S. Y., Via, L. E., Barry, C. E., Klein, E., Kirschner, D. E., et al. (2013) · The Journal of Immunology · doi:10.4049/jimmunol.1300113 · Cited by 347
IL-10 Blocks Phagosome Maturation in Mycobacterium tuberculosis– Infected Human Macrophages
O'Leary, S., O'Sullivan, M. P., & Keane, J. (2011) · American Journal of Respiratory Cell and Molecular Biology · doi:10.1165/rcmb.2010-0319oc · Cited by 229
Metadata
- Authors
- Schreiber, T., Ehlers, S., Heitmann, L., Rausch, A., Mages, J., Murray, P. J., Lang, R., & Hölscher, C.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- 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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