Modulation of murine macrophage function by IL-13
Abstract
Activated macrophages are important effector cells for immune response to many parasites and immune responses are strongly modulated in part by the effect of Th cell-derived cytokines on macrophages. Th1-derived cytokines such as IFN-gamma are strong stimulators of macrophage activation, while cytokines produced by Th2 cells, including IL-4 and IL-10, have been shown under some conditions to inhibit macrophage activities associated with inflammatory responses. IL-13, a recently described cytokine produced by Th2 cells, is also capable of down-modulating macrophage activity in a manner similar to that previously described for IL-4. Treatment of activated macrophages with IL-13 reduces the production of inflammatory monokines in response to IFN-gamma or LPS, both potent stimulators of these factors. In addition, IL-13 decreases the production of nitric oxide by activated macrophages. Nitric oxide has been implicated in both macrophage cytotoxicity and macrophage-associated immunosuppression. The suppression of nitric oxide by IL-13 leads to a decrease in parasiticidal activity by activated macrophages. However, our data indicate that IL-13 has pleiotropic effects, while the inflammatory potential of activated macrophages is significantly reduced, the potential of other macrophage subsets is unimpaired. These data indicate that IL-13 could be a potent modulator of immune responses in vivo, with effects that may embrace both macrophage suppressive and macrophage potentiating functions.
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Alternatively activated macrophages do not require priming because IL-4 and/or IL-13 can act as sufficient stimuli.
“Alternatively activated macrophages do not require any priming, because interleukins IL-4 and/or IL-13 can act as enough stimuli [190,191].”
From Superoxide Anion Chemistry—Its Role at the Core of the Innate Immunity (2023) · cites this paper as [191]
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Enhanced protection from fibrosis and inflammation in the combined absence of IL‐13 and IFN ‐γ
Ramalingam, T. R., Gieseck, R. L., Acciani, T. H., Hart, K. M., Cheever, A. W., Mentink‐Kane, M. M., Vannella, K. M., & Wynn, T. A. (2016) · The Journal of Pathology · doi:10.1002/path.4733 · Cited by 57 · see citing works
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- Authors
- Doherty, T. M., Kastelein, R., Menon, S., Andrade, S., & Coffman, R. L.
- Affiliations
- Department of Immunology, DNAX Research Institute for Cellular and Molecular Biology , Palo Alto, CA 94304
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 1993-12
- Volume
- 151
- Issue
- 12
- Pages
- 7151-7160
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1537669972
- Cited by
- 249
- References
- 0
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 2 · 2023: 6 · 2022: 3 · 2021: 5 · 2020: 4 · 2019: 8 · 2018: 1 · 2017: 5 · 2016: 7 · 2015: 7 · 2014: 6 · 2013: 3 · 2012: 3
- FWCI
- 5.53
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- IL-13, macrophage activation, Th2 cytokines, nitric oxide, macrophage cytotoxicity, antiparasitic activity, interferon-gamma, LPS, immunosuppression, Th1/Th2 balance, macrophage subsets
- MeSH terms
- Animals, Antigens, Surface, Cytotoxicity, Immunologic, Female, Interleukins, Macrophage Activation, Macrophages, Male, Mice, Inbred BALB C, Mice, Inbred C57BL, Phagocytosis, Cytokines, Antigen Presentation, Interleukin-13, Mice, In Vitro Techniques
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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