The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Autocrine Deactivation of Macrophages in Transgenic Mice Constitutively Overexpressing IL-10 Under Control of the Human CD68 Promoter
Abstract
IL-10 plays an essential role in blocking cytokine production by activated macrophages. To analyze the consequences of enforced expression of IL-10 by macrophages on innate and adaptive immune responses, we generated transgenic mice (macIL-10tg mice) expressing an epitope-tagged IL-10 (Flag-IL-10) under control of the human CD68 promoter. Expression of Flag-IL-10 was constitutive and restricted to macrophages, as shown by sorting splenocyte cell populations and intracellular staining for IL-10. Transgenic macrophages displayed suppressed production of TNF-α and IL-12 upon stimulation with LPS. When macIL-10tg mice were challenged with LPS, serum levels of proinflammatory cytokines were attenuated compared with controls. Infection with Mycobacterium bovis bacille Calmette-Guérin resulted in ∼10-fold-higher bacterial loads than in wild-type mice. Normal T and B cell responses were observed in macIL-10tg mice, suggesting that macrophage-specific overexpression of IL-10 predominantly acts in an autocrine/paracrine manner, resulting in chronically deactivated macrophages that manifest an impaired ability to control pathogens.
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Cites
Interleukin-10 and the Interleukin-10 Receptor
Moore, K. W., de Waal Malefyt, R., Coffman, R. L., & O'Garra, A. (2001) · Annual Review of Immunology · doi:10.1146/annurev.immunol.19.1.683 · Cited by 6,737
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The role of IL-10 in promoting disease progression in Leishmaniasis
Kane, M. M., & Mosser, D. M. (2001) · The Journal of Immunology · doi:10.4049/jimmunol.166.2.1141 · Cited by 514
Jin, D. I., Jameson, S. B., Reddy, M. A., Schenkman, D., & Ostrowski, M. C. (1995) · Molecular and Cellular Biology · doi:10.1128/mcb.15.2.693 · Cited by 47
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Gordon, S. (2003) · Nature Reviews Immunology · doi:10.1038/nri978 · Cited by 6,189
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Vats, D., Mukundan, L., Odegaard, J. I., Zhang, L., Smith, K. L., Morel, C. R., Greaves, D. R., Murray, P. J., & Chawla, A. (2006) · Cell Metabolism · doi:10.1016/j.cmet.2006.05.011 · Cited by 1,369
Self-citationUnderstanding and exploiting the endogenous interleukin-10/STAT3-mediated anti-inflammatory response
MURRAY, P. (2006) · Current Opinion in Pharmacology · doi:10.1016/j.coph.2006.01.010 · Cited by 436
Self-citationMAP kinase phosphatase 1 controls innate immune responses and suppresses endotoxic shock
Zhao, Q., Wang, X., Nelin, L. D., Yao, Y., Matta, R., Manson, M. E., Baliga, R. S., Meng, X., Smith, C. V., Bauer, J. A., et al. (2006) · The Journal of Experimental Medicine · doi:10.1084/jem.20051794 · Cited by 370
Schizophrenia and autism: both shared and disorder-specific pathogenesis via perinatal inflammation?
MEYER, U., FELDON, J., & DAMMANN, O. (2011) · Pediatric Research · doi:10.1203/pdr.0b013e318212c196 · Cited by 357
“However, we would like to emphasize that enhanced anti-inflammatory and immunosuppressive actions may increase the sensitivity to infections (77), and this may act in concert with the presence of latent immune abnormalities (induced by perinatal immune priming) in the development of altered inflammatory responses in p…”
Metadata
- Authors
- Lang, R., Rutschman, R. L., Greaves, D. R., & Murray, P. J.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2002-04-01
- Volume
- 168
- Issue
- 7
- Pages
- 3402-3411
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1755443043
- Cited by
- 169
- References
- 4
- FWCI
- 3.38
- Type
- journal article
- Language
- en
- Open access
- closed
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- Lang, R., Rutschman, R. L., Greaves, D. R., & Murray, P. J. (2002). Autocrine Deactivation of Macrophages in Transgenic Mice Constitutively Overexpressing IL-10 Under Control of the Human CD68 Promoter. The Journal of Immunology. https://doi.org/10.4049/jimmunol.168.7.3402
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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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