The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.
Human macrophage activation programs induced by bacterial pathogens
Abstract
Understanding the response of innate immune cells to pathogens may provide insights to host defenses and the tactics used by pathogens to circumvent these defenses. We used DNA microarrays to explore the responses of human macrophages to a variety of bacteria. Macrophages responded to a broad range of bacteria with a robust, shared pattern of gene expression. The shared response includes genes encoding receptors, signal transduction molecules, and transcription factors. This shared activation program transforms the macrophage into a cell primed to interact with its environment and to mount an immune response. Further study revealed that the activation program is induced by bacterial components that are Toll-like receptor agonists, including lipopolysaccharide, lipoteichoic acid, muramyl dipeptide, and heat shock proteins. Pathogen-specific responses were also apparent in the macrophage expression profiles. Analysis of Mycobacterium tuberculosis -specific responses revealed inhibition of interleukin-12 production, suggesting one means by which this organism survives host defenses. These results improve our understanding of macrophage defenses, provide insights into mechanisms of pathogenesis, and suggest targets for therapeutic intervention.
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“Despite a number of genomic studies analyzing macrophage activation in response to bacteria, TLR ligands, and M1 or M2 stimuli, to date there have been no attempts to reconcile these observations by building new and integrative models of macrophage activation”
From Transcriptome-Based Network Analysis Reveals a Spectrum Model of Human Macrophage Activation (2014) · cites this paper as Nau et al., 2002
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Cites
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Defective LPS Signaling in C3H/HeJ and C57BL/10ScCr Mice: Mutations in Tlr4 Gene
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Toll-like receptors: critical proteins linking innate and acquired immunity
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Expression monitoring by hybridization to high-density oligonucleotide arrays
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Toll-like Receptor-4 Mediates Lipopolysaccharide-induced Signal Transduction
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Cited by
Alternative activation of macrophages
Gordon, S. (2003) · Nature Reviews Immunology · doi:10.1038/nri978 · Cited by 6,189
The M1 and M2 paradigm of macrophage activation: Time for reassessment
Martinez, F. O., & Gordon, S. (2014) · F1000Prime Reports · doi:10.12703/p6-13 · Cited by 4,689
Macrophages, inflammation, and insulin resistance
Olefsky, J. M., & Glass, C. K. (2010) · Annual Review of Physiology · doi:10.1146/annurev-physiol-021909-135846 · Cited by 2,733
Transcriptional regulation of macrophage polarization: enabling diversity with identity
Lawrence, T., & Natoli, G. (2011) · Nature Reviews Immunology · doi:10.1038/nri3088 · Cited by 2,284
Transcriptome-Based Network Analysis Reveals a Spectrum Model of Human Macrophage Activation
Xue, J., Schmidt, S. V., Sander, J., Draffehn, A., Krebs, W., Quester, I., De Nardo, D., Gohel, T. D., Emde, M., Schmidleithner, L., et al. (2014) · Immunity · doi:10.1016/j.immuni.2014.01.006 · Cited by 2,210
Metadata
- Authors
- Nau, G. J., Richmond, J. F. L., Schlesinger, A., Jennings, E. G., Lander, E. S., & Young, R. A.
- Affiliations
- Whitehead Institute, 9 Cambridge Center, Cambridge, MA 02142; Infectious Disease Unit, Massachusetts General Hospital, Boston, MA 02114; and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2002-01-22
- Volume
- 99
- Issue
- 3
- Pages
- 1503-1508
- ISSN
- 0027-8424
- 1091-6490
- Cited by
- 568
- References
- 32
- Language
- en
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- Nau, G. J., Richmond, J. F. L., Schlesinger, A., Jennings, E. G., Lander, E. S., & Young, R. A. (2002). Human macrophage activation programs induced by bacterial pathogens. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.022649799
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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.
