The DOI matches its Crossref record; 21 of the 21 references it cites were found in a registry or an index.
Interleukin 4 potently enhances murine macrophage mannose receptor activity: A marker of alternative immunologic macrophage activation
Open accessAbstract
Expression of the macrophage mannose receptor is inhibited by interferon gamma (IFN-gamma), a T helper type 1 (Th-1)-derived lymphokine. Interleukin 4 (IL-4), a Th-2 lymphocyte product, upregulates major histocompatibility class II antigen expression but inhibits inflammatory cytokine production by macrophages. We have studied the effect of IL-4 on expression of the macrophage mannose receptor (MMR) by elicited peritoneal macrophages. We found that recombinant murine IL-4 enhances MMR surface expression (10-fold) and activity (15-fold), as measured by the respective binding and degradation of 125I-mannose-bovine serum albumin. Polymerase chain reaction analysis of cDNAs from purified primary macrophage populations revealed that MMR, but not lysozyme or tumor necrosis factor alpha, mRNA levels were markedly increased by IL-4. The above effects were associated with morphologic changes. These data establish IL-4 as a potent and selective enhancer of murine MMR activity in vitro. IL-4 induces inflammatory macrophages to adopt an alternative activation phenotype, distinct from that induced by IFN-gamma, characterized by a high capacity for endocytic clearance of mannosylated ligands, enhanced (albeit restricted) MHC class II antigen expression, and reduced proinflammatory cytokine secretion.
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“Alternatively activated macrophages are stimulated by IL-4, IL-13 and glucocorticoids, inhibit pro-inflammatory cytokines, promote anti-inflammatory cytokines, and upregulate mannose receptors.[123, 124]”
From Foreign body reaction to biomaterials (2008) · cites this paper as [123]
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“Later during the healing process, macrophages transit from a pro-inflammatory M1 to a reparative M2 phenotype, expressing anti-inflammatory mediators, e.g., IL-1R antagonist, decoy IL-1 receptor type II and IL-10, and growth factors, e.g., TGFβ, VEGF and IGF1, promoting fibroblast proliferation, ECM synthesis and angiogenesis (Fig. 2) [59, 60].”
From Transition from inflammation to proliferation: a critical step during wound healing (2016) · cites this paper as [60]
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“A phenotypic switch in biomaterial adherent macrophages to a more alternatively activated macrophage phenotype over time is expected because in order to induce fusion IL-4 is added to our culture system on days 3 and 7[58] IL-4 is known to induce an alternative activation phenotype in macrophages inclusive of the upregulation of mannose receptors[123] which has been found to be necessary for the”
From Foreign body reaction to biomaterials (2008) · cites this paper as [123]
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“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 [190]
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Citations
Cites
Interferon-γ and B Cell Stimulatory Factor-1 Reciprocally Regulate Ig Isotype Production
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Self-citationCrawford, R. M., Finbloom, D. S., Ohara, J., et al. (1987) · The Journal of Immunology · doi:10.4049/jimmunol.139.1.135 · Cited by 301
Modulation of phenotypic and functional properties of human peripheral blood monocytes by IL-4.
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Cross, M. A., Mangelsdorf, I., Wedel, A., & Renkawitz, R. (1988) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.85.17.6232 · Cited by 260
IL-4 inhibits the expression of IL-8 from stimulated human monocytes.
Standiford, T. J., Strieter, R. M., Chensue, S. W., Westwick, J. K., Kasahara, K., & Kunkel, S. L. (1990) · The Journal of Immunology · doi:10.4049/jimmunol.145.5.1435 · Cited by 238
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Abramson, S., & Gallin, J. (1990) · Journal of Immunology · doi:10.4049/jimmunol.144.2.625 · Cited by 215
Interleukin 4 down‐regulates the expression of CD14 in normal human monocytes
Lauener, R. P., Goyert, S. M., Geha, R. S., et al. (1990) · European Journal of Immunology · doi:10.1002/eji.1830201103 · Cited by 157
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Garcia-Flores, V., Romero, R., Miller, D., Xu, Y., Done, B., Veerapaneni, C., Leng, Y., Arenas-Hernandez, M., Khan, N., Panaitescu, B., et al. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.01291 · Cited by 71
Site-specific subtypes of macrophages recruited after peripheral nerve injury
Komori, T., Morikawa, Y., Inada, T., Hisaoka, T., & Senba, E. (2011) · Neuroreport · doi:10.1097/wnr.0b013e32834cd76a · Cited by 71
McNally, A. K., & Anderson, J. M. (2003) · The American Journal of Pathology · doi:10.1016/s0002-9440(10)63474-8 · Cited by 69
MLean, N. A., & Verge, V. M. K. (2016) · Glia · doi:10.1002/glia.23021 · Cited by 62
Involvement of IGF-1 and Akt in M1/M2 activation state in bone marrow-derived macrophages
Barrett, J. P., Minogue, A. M., Falvey, A., & Lynch, M. A. (2015) · Experimental Cell Research · doi:10.1016/j.yexcr.2015.05.015 · Cited by 59
Macrophage diversity in cardiac inflammation: A review
Barin, J. G., Rose, N. R., & Čiháková, D. (2012) · Immunobiology · doi:10.1016/j.imbio.2011.06.009 · Cited by 56
“The activation of macrophages by IL4 was demonstrated in 1992 by Stein and colleagues, who reported that IL4 induced the expression of macrophage mannose receptor (MφMR, CD206), upregulation of MHC Class II, proliferation, and syncytiation in macrophages (25).”
BackgroundTumor-associated macrophages: Prognostic and therapeutic targets for cancer in humans and dogs
Brady, R. V., & Thamm, D. H. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1176807 · Cited by 35
Naglik, J. R. (2014) · New Journal of Science · doi:10.1155/2014/390241 · Cited by 29
Collagen morphology influences macrophage shape and marker expression in?vitro
Vasse, G. F., Kühn, P. T., Zhou, Q., Bhusari, S. A., Reker-Smit, C., Melgert, B. N., & van Rijn, P. (2018) · Journal of Immunology and Regenerative Medicine · doi:10.1016/j.regen.2018.01.002 · Cited by 25
Novel grooved substrata stimulate macrophage fusion, CCL2 and MMP‐9 secretion
Moon, H., Cremmel, C. V. M., Kulpa, A., Jaeger, N. A. F., Kappelhoff, R., Overall, C. M., Waterfield, J. D., & Brunette, D. M. (2016) · Journal of Biomedical Materials Research Part A · doi:10.1002/jbm.a.35757 · Cited by 14
Ahmed, A. M. M., Bomford, A., Nouri-Aria, K. T., Davies, T., Smith, R., & Williams, R. (2011) · Results in Immunology · doi:10.1016/j.rinim.2011.08.004 · Cited by 11
Metadata
- Authors
- Stein, M., Keshav, S., Harris, N., & Gordon, S.
- Affiliations
- University of Oxford (GB)
- Venue
- The Journal of experimental medicine
- Publisher
- Rockefeller University Press
- Published
- 1992-07-01
- Volume
- 176
- Issue
- 1
- Pages
- 287-292
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC2119288
- OpenAlex
- W2123640179
- Cited by
- 1,960
- References
- 21
- Citations by year
- 2026: 48 · 2025: 66 · 2024: 74 · 2023: 80 · 2022: 115 · 2021: 102 · 2020: 92 · 2019: 93 · 2018: 94 · 2017: 106 · 2016: 116 · 2015: 110 · 2014: 137 · 2013: 100 · 2012: 88
- FWCI
- 2.90
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- cc-by-nc-sa
- Locations
- The Journal of Experimental Medicine (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- IL-4, CD206, alternative macrophage activation, interferon-gamma, peritoneal macrophages, mannose binding, MHC class II antigen expression, proinflammatory cytokine secretion
- MeSH terms
- Mannose Receptor, Animals, Base Sequence, Interferon-gamma, Macrophage Activation, Macrophages, Male, Mannose, Mice, Inbred BALB C, Molecular Sequence Data, Receptors, Cell Surface, Receptors, Immunologic, RNA, Messenger, Interleukin-4, Lectins, C-Type, Mannose-Binding Lectins, Mice
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