The DOI matches its Crossref record; 47 of the 47 references it cites were found in a registry or an index.
Metabolic Reprogramming Mediated by the mTORC2-IRF4 Signaling Axis Is Essential for Macrophage Alternative Activation
Open accessAbstract
Changes in metabolism can be initiated in response to signals received from other cells. An example of this is provided by macrophages that have been stimulated by IL-4 to become alternatively/M2 activated. In these cells, fatty acid oxidation is increased and this is critical for M2 activation. Compared to resting macrophages, M2 macrophages also exhibit changes in glucose metabolism that we have found are essential for activation. In other cell types, mTORC2 has been linked to enhanced glycolysis. We have found that mTORC2 operates in parallel with the IL-4Rα/Stat6 pathway to facilitate increased glycolysis during M2 activation. Our data strongly implicate PI3K and AKT signaling initiated by M-CSF as components in this pathway, and indicate that downstream induction of IRF4 expression plays a role in metabolic reprograming to support M2 activation. We show that loss of mTORC2 in macrophages suppresses tumor growth and decreases immunity to a parasitic nematode.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Macrophage activation and polarization: nomenclature and experimental guidelines
Murray, P. J., Allen, J. E., Biswas, S. K., Fisher, E. A., Gilroy, D. W., Goerdt, S., Gordon, S., Hamilton, J. A., Ivashkiv, L. B., Lawrence, T., et al. (2014) · Immunity · doi:10.1016/j.immuni.2014.06.008 · Cited by 6,337
Macrophage biology in development, homeostasis and disease
Wynn, T. A., Chawla, A., & Pollard, J. W. (2013) · Nature · doi:10.1038/nature12034 · Cited by 4,684 · cited 4×
“The ability of these cells to serve multiple functions reflects their ability to express different genes in response to distinct extracellular signals, including pathogen- and damage- associated molecular patterns and cytokines (Glass and Natoli, 2016; Wynn et al., 2013).”
InfluentialTumor-Associated Macrophages: From Mechanisms to Therapy
Noy, R., & Pollard, J. W. (2014) · Immunity · doi:10.1016/j.immuni.2014.06.010 · Cited by 4,089
Metabolic Competition in the Tumor Microenvironment Is a Driver of Cancer Progression
Chang, C.-H., Qiu, J., O’Sullivan, D., Buck, M. D., Noguchi, T., Curtis, J. D., Chen, Q., Gindin, M., Gubin, M. M., van der Windt, G. J. W., et al. (2015) · Cell · doi:10.1016/j.cell.2015.08.016 · Cited by 3,331
Self-citationCSF-1R inhibition alters macrophage polarization and blocks glioma progression
Pyonteck, S. M., Akkari, L., Schuhmacher, A. J., Bowman, R. L., Sevenich, L., Quail, D. F., Olson, O. C., Quick, M. L., Huse, J. T., Teijeiro, V., et al. (2013) · Nature Medicine · doi:10.1038/nm.3337 · Cited by 2,463
Jha, A. K., Huang, S. C.-C., Sergushichev, A., Lampropoulou, V., Ivanova, Y., Loginicheva, E., Chmielewski, K., Stewart, K. M., Ashall, J., Everts, B., et al. (2015) · Immunity · doi:10.1016/j.immuni.2015.02.005 · Cited by 2,066
Self-citationImmunometabolism governs dendritic cell and macrophage function
O’Neill, L. A. J., & Pearce, E. J. (2016) · Journal of Experimental Medicine · doi:10.1084/jem.20151570 · Cited by 1,694
Self-citationOxidative metabolism and PGC-1β attenuate macrophage-mediated inflammation
Vats, D., Mukundan, L., Odegaard, J. I., Zhang, L., Smith, K. L., Morel, C. R., Greaves, D. R., Murray, P. J., & Chawla, A. (2006) · Cell Metabolism · doi:10.1016/j.cmet.2006.05.011 · Cited by 1,369 · cited 3×
“For example, in macrophages stimulated by IL-4 to become alternatively activated, FAO increases to support OXPHOS, and these processes are critical for full M2 activation (Huang et al., 2014; Vats et al., 2006).”
The mTOR Kinase Differentially Regulates Effector and Regulatory T Cell Lineage Commitment
Delgoffe, G. M., Kole, T. P., Zheng, Y., Zarek, P. E., Matthews, K. L., Xiao, B., Worley, P. F., Kozma, S. C., & Powell, J. D. (2009) · Immunity · doi:10.1016/j.immuni.2009.04.014 · Cited by 1,284
Regulation of the mTOR Complex 1 Pathway by Nutrients, Growth Factors, and Stress
Sengupta, S., Peterson, T. R., & Sabatini, D. M. (2010) · Molecular Cell · doi:10.1016/j.molcel.2010.09.026 · Cited by 1,241
Research works printed but not linked: 1
- Masui, 2014, mTORC2 dictates Warburg effect and drug resistance, Cell Cycle, 13, 1053, 10.4161/cc.28377 · doi:10.4161/cc.28377
Cited by
PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer
Glaviano, A., Foo, A. S. C., Lam, H. Y., Yap, K. C. H., Jacot, W., Jones, R. H., Eng, H., Nair, M. G., Makvandi, P., Geoerger, B., et al. (2023) · Molecular Cancer · doi:10.1186/s12943-023-01827-6 · Cited by 2,138
The metabolic signature of macrophage responses
Viola, A., Munari, F., Sánchez-Rodríguez, R., Scolaro, T., & Castegna, A. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.01462 · Cited by 2,021
α-ketoglutarate orchestrates macrophage activation through metabolic and epigenetic reprogramming
Liu, P.-S., Wang, H., Li, X., Chao, T., Teav, T., Christen, S., Di Conza, G., Cheng, W.-C., Chou, C.-H., Vavakova, M., et al. (2017) · Nature Immunology · doi:10.1038/ni.3796 · Cited by 1,264
Macrophage Immunometabolism: Where Are We (Going)?
Van den Bossche, J., O’Neill, L. A., & Menon, D. (2017) · Trends in Immunology · doi:10.1016/j.it.2017.03.001 · Cited by 1,163
Targeting tumor-associated macrophages in cancer
Pathria, P., Louis, T. L., & Varner, J. A. (2019) · Trends in Immunology · doi:10.1016/j.it.2019.02.003 · Cited by 933
Metadata
- Authors
- Huang, S. C.-C., Smith, A. M., Everts, B., Colonna, M., Pearce, E. L., Schilling, J. D., & Pearce, E. J.
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2016-10
- Volume
- 45
- Issue
- 4
- Pages
- 817-830
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W2534854440
- Cited by
- 667
- References
- 47
- FWCI
- 25.40
- Type
- journal article
- Language
- en
- Open access
- bronze
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 382 d)
- Funders
- NIH (AI110481, CA164062, CA18112502, P30 DK020579)
- NWO (VENI-91614087)
- Marie Curie (CIG-631585)
- American Heart Association (14POST20480221)
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Metabolic Reprogramming Mediated by the mTORC2-IRF4 Signaling Axis Is Essential for Macrophage Alternative Activation. https://app.cochat.ai/papers/10.1016/j.immuni.2016.09.016
- The paper
- Huang, S. C.-C., Smith, A. M., Everts, B., Colonna, M., Pearce, E. L., Schilling, J. D., & Pearce, E. J. (2016). Metabolic Reprogramming Mediated by the mTORC2-IRF4 Signaling Axis Is Essential for Macrophage Alternative Activation. Immunity. https://doi.org/10.1016/j.immuni.2016.09.016
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
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.