The DOI matches its Crossref record; 63 of the 63 references it cites were found in a registry or an index.
IL-4 directly signals tissue-resident macrophages to proliferate beyond homeostatic levels controlled by CSF-1
Open accessAbstract
Macrophages (MΦs) colonize tissues during inflammation in two distinct ways: recruitment of monocyte precursors and proliferation of resident cells. We recently revealed a major role for IL-4 in the proliferative expansion of resident MΦs during a Th2-biased tissue nematode infection. We now show that proliferation of MΦs during intestinal as well as tissue nematode infection is restricted to sites of IL-4 production and requires MΦ-intrinsic IL-4R signaling. However, both IL-4Rα–dependent and –independent mechanisms contributed to MΦ proliferation during nematode infections. IL-4R–independent proliferation was controlled by a rise in local CSF-1 levels, but IL-4Rα expression conferred a competitive advantage with higher and more sustained proliferation and increased accumulation of IL-4Rα+ compared with IL-4Rα− cells. Mechanistically, this occurred by conversion of IL-4Rα+ MΦs from a CSF-1–dependent to –independent program of proliferation. Thus, IL-4 increases the relative density of tissue MΦs by overcoming the constraints mediated by the availability of CSF-1. Finally, although both elevated CSF1R and IL-4Rα signaling triggered proliferation above homeostatic levels, only CSF-1 led to the recruitment of monocytes and neutrophils. Thus, the IL-4 pathway of proliferation may have developed as an alternative to CSF-1 to increase resident MΦ numbers without coincident monocyte recruitment.
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Cites
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“…elevated tissue M density during infection through additional cellintrinsic mech anisms, for example, by reducing reliance on local glucose levels (Vats et al., 2006), inhibiting migration from the tissue induced the recruitment of inflammatory cells including neu trophils and Ly6C+ monocytes…”
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Cited by
Macrophages in Tissue Repair, Regeneration, and Fibrosis
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Metadata
- Authors
- Jenkins, S. J., Ruckerl, D., Thomas, G. D., Hewitson, J. P., Duncan, S., Brombacher, F., Maizels, R. M., Hume, D. A., & Allen, J. E.
- Venue
- Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2013-10-07
- Volume
- 210
- Issue
- 11
- Pages
- 2477-2491
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2153846543
- Cited by
- 401
- References
- 63
- FWCI
- 17.30
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Jenkins, S. J., Ruckerl, D., Thomas, G. D., Hewitson, J. P., Duncan, S., Brombacher, F., Maizels, R. M., Hume, D. A., & Allen, J. E. (2013). IL-4 directly signals tissue-resident macrophages to proliferate beyond homeostatic levels controlled by CSF-1. Journal of Experimental Medicine. https://doi.org/10.1084/jem.20121999
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