The DOI matches its Crossref record; 50 of the 50 references it cites were found in a registry or an index.
Toll-like receptor–induced arginase 1 in macrophages thwarts effective immunity against intracellular pathogens
Open accessAbstract
Toll-like receptor (TLR) signaling in macrophages is required for antipathogen responses, including the biosynthesis of nitric oxide from arginine, and is essential for immunity to Mycobacterium tuberculosis, Toxoplasma gondii and other intracellular pathogens. Here we report a 'loophole' in the TLR pathway that is advantageous to these pathogens. Intracellular pathogens induced expression of the arginine hydrolytic enzyme arginase 1 (Arg1) in mouse macrophages through the TLR pathway. In contrast to diseases dominated by T helper type 2 responses in which Arg1 expression is greatly increased by interleukin 4 and 13 signaling through the transcription factor STAT6, TLR-mediated Arg1 induction was independent of the STAT6 pathway. Specific elimination of Arg1 in macrophages favored host survival during T. gondii infection and decreased lung bacterial load during tuberculosis infection.
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“Consequently, mice deficient in Arg1 are better protected against M. tuberculosis infection (108).”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [108]
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“In contrast, arginase-1, which depletes the Nos2 substrate arginine by converting it to ornithine [62, 205], is reduced by heme.”
From “Pumping iron”—how macrophages handle iron at the systemic, microenvironmental, and cellular levels (2017) · cites this paper as [62]
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Citations
Cites
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An Effect of Parasite-Encoded Arginase on the Outcome of Murine Cutaneous Leishmaniasis
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Macrophage activation and polarization: nomenclature and experimental guidelines
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“…has led to interpretive problems because Arg1 is also induced in M1 spectrum macrophages, expressed in some resident macrophage populations, and highly induced in mycobacteria-infected macrophages, further emphasizing the need for criteria encompassing multiple markers (El Kasmi et al., 2008).”
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“There are obvious caveats to the use of reverse analysis alone, as required in human studies in situ: substantial species differences exist in available markers, and established markers such as Arg1 can be induced by other pathways (El Kasmi et al., 2008).”
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“F or p er so na l u se o nl y. Table 1 (Continued ) Protein (gene)a Function Genetic lesionb Effect on polarization Reference(s) Notes IRF5 (Irf5) Transcription factor Conditional knockout (LysM-Cre) Complete knockout Loss of M1 65, 106 None TSC1 (Tsc1) Inhibitor of mTOR Conditional knockout (LysM-Cre) Gain of M1 Part…”
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“Both STAT6 and C/EBPβ have recently been shown to be essential for arginase 1 expression in macrophages, but in a stimulus-specific manner owing to the selective use of distinct cis -acting elements in the Arg1 promote”
Background
Metadata
- Authors
- El Kasmi, K. C., Qualls, J. E., Pesce, J. T., Smith, A. M., Thompson, R. W., Henao-Tamayo, M., Basaraba, R. J., König, T., Schleicher, U., Koo, M.-S., Kaplan, G., Fitzgerald, K. A., Tuomanen, E. I., Orme, I. M., Kanneganti, T.-D., Bogdan, C., Wynn, T. A., & Murray, P. J.
- Affiliations
- St. Jude Children's Research Hospital (US)
- National Institutes of Health (US)
- Colorado State University (US)
- University Medical Center Freiburg (DE)
- Universitätsklinikum Erlangen (DE)
- University of Medicine and Dentistry of New Jersey (US)
- University of Massachusetts Chan Medical School (US)
- Corresponding author
- Wynn, Thomas A
- Murray, Peter J
- ORCID
- Venue
- Nature Immunology
- Published
- 2008-11-02
- Volume
- 9
- Issue
- 12
- Pages
- 1399-1406
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- PMC
- PMC2584974
- OpenAlex
- W2038461328
- Cited by
- 646
- References
- 50
- Citations by year
- 2026: 18 · 2025: 20 · 2024: 19 · 2023: 33 · 2022: 25 · 2021: 48 · 2020: 34 · 2019: 35 · 2018: 32 · 2017: 29 · 2016: 52 · 2015: 51 · 2014: 52 · 2013: 49 · 2012: 39
- FWCI
- 13.66
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship@UMassChan (submittedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (P30CA021765)
- National Institute of Allergy and Infectious Diseases (AI27913, R01AI027913, AI062921, R01AI066046, AI66046, R01AI062921)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Health Sciences › Medicine › Infectious Diseases › Tuberculosis Research and Epidemiology
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Keywords
- arginase-1, Toll-like receptor signaling, macrophages, intracellular pathogens, Mycobacterium tuberculosis, Toxoplasma gondii, nitric oxide, STAT6, host-pathogen interaction, tuberculosis, toxoplasmosis, lung bacterial load
- MeSH terms
- Animals, Arginase, Bacterial Infections, Immunohistochemistry, Macrophages, Immunoblotting, Mice, Knockout, CCAAT-Enhancer-Binding Protein-beta, STAT6 Transcription Factor, Toll-Like Receptors, Mice, Myeloid Differentiation Factor 88
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