Cited by 1,191Multiple Sclerosis Research StudiesPsoriasis: Treatment and PathogenesisT-cell and B-cell Immunology

The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index.

RORγt drives production of the cytokine GM-CSF in helper T cells, which is essential for the effector phase of autoimmune neuroinflammation

Codarri, Laura, Gyülvészi, Gabor, Tosevski, Vinko, Hesske, Lysann, Fontana, Adriano, Magnenat, Laurent, Suter, Tobias, Becher, Burkhard·2011·Nature Immunology

DOI 10.1038/ni.2027

Open this paper in CoChat — free account

Abstract

Although the role of the T(H)1 and T(H)17 subsets of helper T cells as disease mediators in autoimmune neuroinflammation remains a subject of some debate, none of their signature cytokines are essential for disease development. Here we report that interleukin 23 (IL-23) and the transcription factor RORγt drove expression of the cytokine GM-CSF in helper T cells, whereas IL-12, interferon-γ (IFN-γ) and IL-27 acted as negative regulators. Autoreactive helper T cells specifically lacking GM-CSF failed to initiate neuroinflammation despite expression of IL-17A or IFN-γ, whereas GM-CSF secretion by Ifng(-/-)Il17a(-/-) helper T cells was sufficient to induce experimental autoimmune encephalomyelitis (EAE). During the disease effector phase, GM-CSF sustained neuroinflammation via myeloid cells that infiltrated the central nervous system. Thus, in contrast to all other known helper T cell-derived cytokines, GM-CSF serves a nonredundant function in the initiation of autoimmune inflammation regardless of helper T cell polarization.

Integrity signals

Registry

Crossref · 10.1038/ni.2027

Cites

44 of 44 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells
Bettelli, E., Carrier, Y., Gao, W., Korn, T., Strom, T. B., Oukka, M., Weiner, H. L., & Kuchroo, V. K. (2006) · Nature · doi:10.1038/nature04753 · Cited by 6,992
The Orphan Nuclear Receptor RORγt Directs the Differentiation Program of Proinflammatory IL-17+ T Helper Cells
Ivanov, I. I., McKenzie, B. S., Zhou, L., Tadokoro, C. E., Lepelley, A., Lafaille, J. J., Cua, D. J., & Littman, D. R. (2006) · Cell · doi:10.1016/j.cell.2006.07.035 · Cited by 5,145
Interleukin 17-producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages
Harrington, L. E., Hatton, R. D., Mangan, P. R., Turner, H., Murphy, T. L., Murphy, K. M., & Weaver, C. T. (2005) · Nature Immunology · doi:10.1038/ni1254 · Cited by 4,742
A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17
Park, H., Li, Z., Yang, X. O., Chang, S. H., Nurieva, R., Wang, Y.-H., Wang, Y., Hood, L., Zhu, Z., Tian, Q., et al. (2005) · Nature Immunology · doi:10.1038/ni1261 · Cited by 4,265
IL-23 drives a pathogenic T cell population that induces autoimmune inflammation
Langrish, C. L., Chen, Y., Blumenschein, W. M., Mattson, J., Basham, B., Sedgwick, J. D., McClanahan, T., Kastelein, R. A., & Cua, D. J. (2005) · The Journal of Experimental Medicine · doi:10.1084/jem.20041257 · Cited by 4,099
TGFβ in the Context of an Inflammatory Cytokine Milieu Supports De Novo Differentiation of IL-17-Producing T Cells
Veldhoen, M., Hocking, R. J., Atkins, C. J., Locksley, R. M., & Stockinger, B. (2006) · Immunity · doi:10.1016/j.immuni.2006.01.001 · Cited by 3,605
Interleukin-23 rather than interleukin-12 is the critical cytokine for autoimmune inflammation of the brain
Cua, D. J., Sherlock, J., Chen, Y., Murphy, C. A., Joyce, B., Seymour, B., Lucian, L., To, W., Kwan, S., Churakova, T., et al. (2003) · Nature · doi:10.1038/nature01355 · Cited by 2,906
Novel p19 Protein Engages IL-12p40 to Form a Cytokine, IL-23, with Biological Activities Similar as Well as Distinct from IL-12
Oppmann, B., Lesley, R., Blom, B., Timans, J. C., Xu, Y., Hunte, B., Vega, F., Yu, N., Wang, J., Singh, K. P., et al. (2000) · Immunity · doi:10.1016/s1074-7613(00)00070-4 · Cited by 2,819
IL-21 initiates an alternative pathway to induce proinflammatory TH17 cells
Korn, T., Bettelli, E., Gao, W., Awasthi, A., Jäger, A., Strom, T. B., Oukka, M., & Kuchroo, V. K. (2007) · Nature · doi:10.1038/nature05970 · Cited by 1,896
Interleukin-23 Promotes a Distinct CD4 T Cell Activation State Characterized by the Production of Interleukin-17
Aggarwal, S., Ghilardi, N., Xie, M.-H., de Sauvage, F. J., & Gurney, A. L. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m207577200 · Cited by 1,848

Show all 44 references

Sorted by citations

Items 301–400 of 1,001

Pathogenic function of bystander-activated memory-like CD4+ T cells in autoimmune encephalomyelitis
Lee, H., Lee, J.-U., Kim, D.-H., Lim, S., Kang, I., & Choi, J. (2019) · Nature Communications · doi:10.1038/s41467-019-08482-w · Cited by 86
NK-DC crosstalk controls the autopathogenic Th17 response through an innate IFN-γ–IL-27 axis
Chong, W. P., van Panhuys, N., Chen, J., Silver, P. B., Jittayasothorn, Y., Mattapallil, M. J., Germain, R. N., & Caspi, R. R. (2015) · The Journal of Experimental Medicine · doi:10.1084/jem.20141678 · Cited by 83
“This was attributed to inhibition of RORt expression, GM-CSF production, enhancement of PD-L1 in T cells and induction of Tr1 cells (Diveu et al., 2009; Murugaiyan et al., 2010; Codarri et al., 2011; Hirahara et al., 2012).”
Interactions between Autophagy and Inhibitory Cytokines
Wu, T., Li, W., & Yao, Y.-M. (2016) · International Journal of Biological Sciences · doi:10.7150/ijbs.15194 · Cited by 84
“Sci. 2016, Vol. 12 http://www.ijbs.com 893 antigen presentation cell; MHC: major histocompatibility complex; STAT: signal transducer and activation of transcription; MAPK: mitogen-activated protein kinase; DC: dendritic cell; GM-CSF: granulocyte-macrophage colony-stimulating factor; Foxp3: Fork head box 3; PBMC: perip…”
Background
Role of Granulocyte-Macrophage Colony-Stimulating Factor Production by T Cells duringMycobacterium tuberculosisInfection
Rothchild, A. C., Stowell, B. L., Goyal, G., Nunes-Alves, C., Yang, Q., Papavinasasundaram, K. G., Sassetti, C. M., Dranoff, G., Chen, X., Lee, J., et al. (2017) · mBio · doi:10.1128/mbio.01514-17 · Cited by 88
The role of T cells in the pathogenesis of Parkinson’s disease
Chen, Z., Chen, S., & Liu, J. (2018) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2018.08.002 · Cited by 81
“Codarri et al. (2011) reported that IL-23 and RORγt drive the expression of GM-CSF, which induces a tremendous Th1 response in EAE and MS (Codarri et al., 2011).”
Background
Graft-versus-host disease, but not graft-versus-leukemia immunity, is mediated by GM-CSF–licensed myeloid cells
Tugues, S., Amorim, A., Spath, S., Martin‐Blondel, G., Schreiner, B., Feo, D. D., Lutz, M., Guscetti, F., Apostolova, P., Haftmann, C., et al. (2018) · Science Translational Medicine · doi:10.1126/scitranslmed.aat8410 · Cited by 80
The Role of Gamma-Delta T Cells in Diseases of the Central Nervous System
Wo, J., Zhang, F., Li, Z., Sun, C., Zhang, W.-C., & Sun, G. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.580304 · Cited by 81
An interferon-β-resistant and NLRP3 inflammasome–independent subtype of EAE with neuronal damage
Inoue, M., Chen, P., Siecinski, S. K., Li, Q.-J., Liu, C., Steinman, L., Gregory, S. G., Benner, E. J., & Shinohara, M. L. (2016) · Nature Neuroscience · doi:10.1038/nn.4421 · Cited by 79
CCR6+ Th cells in the cerebrospinal fluid of persons with multiple sclerosis are dominated by pathogenic non-classic Th1 cells and GM-CSF-only-secreting Th cells
Restorick, S. M., Durant, L., Kalra, S., Hassan‐Smith, G., Rathbone, E. J., Douglas, M. R., & Curnow, J. (2017) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2017.03.008 · Cited by 82
Nanomodulation of Macrophages in Multiple Sclerosis
Nally, F. K., Santi, C. D., & McCoy, C. E. (2019) · Cells · doi:10.3390/cells8060543 · Cited by 80
“GM-CSF is a cytokine produced by Th subsets, and is essential to disease development [62,63].”
Background
A molecular network regulating the proinflammatory phenotype of human memory T lymphocytes
Emming, S., Bianchi, N., Polletti, S., Balestrieri, C., Leoni, C., Montagner, S., Chirichella, M., Delaleu, N., Natoli, G., & Monticelli, S. (2020) · Nature Immunology · doi:10.1038/s41590-020-0622-8 · Cited by 76
GM-CSF contributes to aortic aneurysms resulting from SMAD3 deficiency
Ye, P., Chen, W., Wu, J., Huang, X., Li, J., Wang, S., Liu, Z., Wang, G., Yang, X. Y., Zhang, P., et al. (2013) · Journal of Clinical Investigation · doi:10.1172/jci67356 · Cited by 79
“IL-1β or IFN-γ deficiency has also been shown to significantly induce GMCSF expression (27, 30, 31), which may explain the disease severity observed in Smad3+/–Ifng–/– mice.”
IL-27p28 inhibits central nervous system autoimmunity by concurrently antagonizing Th1 and Th17 responses
Chong, W. P., Horai, R., Mattapallil, M. J., Silver, P. B., Chen, J., Zhou, R., Sergeev, Y. V., Villasmil, R., Chan, C., & Caspi, R. R. (2013) · Journal of Autoimmunity · doi:10.1016/j.jaut.2013.08.003 · Cited by 81
“GM-CSF has recently been identified as the shared effector molecule of both Th1 and Th17 effector CD4+ T cells that are responsible for the pathology of EAE [27,28].”
BackgroundInfluential
Inflammasome activation in obesity-related inflammatory diseases and autoimmunity.
Lukens, J. R., Dixit, V. D., & Kanneganti, T. (2011) · PubMed · Cited by 79
Communication between pathogenic T cells and myeloid cells in neuroinflammatory disease
Deak, L. C., Greter, M., & Becher, B. (2012) · Trends in Immunology · doi:10.1016/j.it.2012.09.007 · Cited by 78
Emerging aspects of cytokine storm in COVID-19: The role of proinflammatory cytokines and therapeutic prospects
Dharra, R., Sharma, A. K., & Datta, S. (2023) · Cytokine · doi:10.1016/j.cyto.2023.156287 · Cited by 82
IL-15 Amplifies the Pathogenic Properties of CD4+CD28− T Cells in Multiple Sclerosis
Broux, B., Mizee, M. R., Vanheusden, M., van der Pol, S. M. A., van Horssen, J., Wijmeersch, B. V., Somers, V. A., de Vries, H. E., Stinissen, P., & Hellings, N. (2015) · The Journal of Immunology · doi:10.4049/jimmunol.1401547 · Cited by 76
“We found that CD4+CD282 T cells produce GM-CSF, but not IL-17A, after stimulation with IL15, either alone or in combination with anti-CD3 (Fig.”
BackgroundInfluential
Identity crisis of Th17 cells: many forms, many functions, many questions
Sundrud, M. S., & Trivigno, C. (2013) · Seminars in Immunology · doi:10.1016/j.smim.2013.10.021 · Cited by 77
“L-23 promotes expression of the non-canonical Th17 cytokine, M-CSF, and this has been shown to be important in EAE pathoenesis [140,141].”
Background
The GM-CSF receptor family: Mechanism of activation and implications for disease
Hercus, T., Broughton, S., Ekert, P., Ramshaw, H., Perugini, M., Grimbaldeston, M., Woodcock, J., Thomas, D., Pitson, S., Hughes, T., et al. (2012) · Growth Factors · doi:10.3109/08977194.2011.649919 · Cited by 73
“…as a hemopoietic CSF (Metcalf 2008), evidence now suggests that GM-CSF plays an important role in signaling emergency myelopoiesis in response to infection and in innate and adaptive immunity (Fleetwood et al. 2005; Shibasaki et al. 2007; Metcalf 2010; Codarri et al. 2011; El-Behi et al. 2011).”
Background
Sphingosine 1 Phosphate at the Blood Brain Barrier: Can the Modulation of S1P Receptor 1 Influence the Response of Endothelial Cells and Astrocytes to Inflammatory Stimuli?
Spampinato, S. F., Obermeier, B., Cotleur, A. C., Love, A. C., Takeshita, Y., Sano, Y., Kanda, T., & Ransohoff, R. M. (2015) · PLoS ONE · doi:10.1371/journal.pone.0133392 · Cited by 77
“In particular, Th1- and Th17-derived GM-CSF triggers recruitment of inflammatory macrophages to the CNS during EAE [59, 60].”
BackgroundInfluential
T-helper cell diversity in experimental autoimmune encephalomyelitis and Multiple Sclerosis
Carbajal, K. S., Mironova, Y. A., Ulrich-Lewis, J. T., Kulkarni, D., Grifka-Walk, H. M., Huber, A. K., Shrager, P., Giger, R., & Segal, B. (2015) · Journal of Immunology · doi:10.4049/jimmunol.1501097 · Cited by 72
Dectin-2 Promotes House Dust Mite–Induced T Helper Type 2 and Type 17 Cell Differentiation and Allergic Airway Inflammation in Mice
Norimoto, A., Hirose, K., Iwata, A., Tamachi, T., Yokota, M., Takahashi, K., Saijo, S., Iwakura, Y., & Nakajima, H. (2014) · American Journal of Respiratory Cell and Molecular Biology · doi:10.1165/rcmb.2013-0522oc · Cited by 76
“Furthermore, freshly isolated MLN CD4(1) T cells from Clec4n mice produced less IL-17A and GM-CSF, recently identified as another effector cytokine produced from Th17 cells (26, 27).”
Background
How Cytokine Networks Fuel Inflammation: Interleukin-17 and a tale of two autoimmune diseases
Baeten, D., & Kuchroo, V. K. (2013) · Nature Medicine · doi:10.1038/nm.3268 · Cited by 75
Circadian clock: a regulator of the immunity in cancer
Zhang, Z., Zeng, P., Gao, W., Zhou, Q., Feng, T., & Tian, X. (2021) · Cell Communication and Signaling · doi:10.1186/s12964-021-00721-2 · Cited by 80
Th17 Cells in Periodontitis and Its Regulation by A20
Huang, N., Dong, H., Luo, Y., & Shao, B. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.742925 · Cited by 84
Effector molecules released by Th1 but not Th17 cells drive an M1 response in microglia
Prajeeth, C. K., Löhr, K., Floess, S., Zimmermann, J., Ulrich, R., Gudi, V., Beineke, A., Baumgärtner, W., Müller, M., Huehn, J., et al. (2014) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2014.01.001 · Cited by 76
CC chemokine receptor 4 is required for experimental autoimmune encephalomyelitis by regulating GM-CSF and IL-23 production in dendritic cells
Poppensieker, K., Otte, D.-M., Schürmann, B., Limmer, A., Dresing, P., Drews, E., Schumak, B., Klotz, L., Raasch, J., Mildner, A., et al. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1114153109 · Cited by 75
“Two recent studies demonstrated that T-cell–derived GM-CSF sustained neuroinflammation via myeloid cells that infiltrated the CNS (41, 42).”
Result
Pathogenic and Protective Functions of TNF in Neuroinflammation Are Defined by Its Expression in T Lymphocytes and Myeloid Cells
Kruglov, A., Lampropoulou, V., Fillatreau, S., & Nedospasov, S. A. (2011) · The Journal of Immunology · doi:10.4049/jimmunol.1100663 · Cited by 75
“Furthermore, GM-CSF production by both Th1 and Th17 cells was reported to be critical for EAE progression via control of myeloid cell accumulation in the CNS (40).”
Background
Group 3 innate lymphoid cells accumulate and exhibit disease-induced activation in the meninges in EAE
Hatfield, J. K., & Brown, M. A. (2015) · Cellular Immunology · doi:10.1016/j.cellimm.2015.06.006 · Cited by 81
Regulation and function of innate and adaptive interleukin‐17‐producing cells
Hirota, K., Ahlfors, H., Duarte, J. H., & Stockinger, B. (2011) · EMBO Reports · doi:10.1038/embor.2011.248 · Cited by 75
“This would change the interpretation of work reported by two independent groups showing that GM-CSF-producing T cells—instead of IFN-γ - producing or IL-17-producing T cells—are a pathogenic subset in EAE (Codarri et al , 2011; El-Behi et al , 2011).”
Posttranscriptional Gene Regulation of IL-17 by the RNA-Binding Protein HuR Is Required for Initiation of Experimental Autoimmune Encephalomyelitis
Chen, J., Cascio, J. A., Magee, J., Techasintana, P., Gubin, M. M., Dahm, G. M., Calaluce, R., Yu, S., & Atasoy, U. (2013) · The Journal of Immunology · doi:10.4049/jimmunol.1301188 · Cited by 76
“The cytokine GM-CSF has also been previously described as playing an important role in the EAE model of multiple sclerosis (27, 35, 36).”
Background
Differentiation and Transmigration of CD4 T Cells in Neuroinflammation and Autoimmunity
Sonar, S. A., & Lal, G. (2017) · Frontiers in Immunology · doi:10.3389/fimmu.2017.01695 · Cited by 73
Innate Immune Modulation by GM-CSF and IL-3 in Health and Disease
Borriello, F., Galdiero, M. R., Varricchi, G., Loffredo, S., Spadaro, G., & Marone, G. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20040834 · Cited by 77
“, Th17 lymphocytes) can produce GM-CSF [26,27], some groups have reported the STAT5-dependent expression of this cytokine by a specialized subset of T cell [29–31].”
Background
Melanoma cell adhesion molecule–positive CD 8 T lymphocytes mediate central nervous system inflammation
Larochelle, C., Lécuyer, M., Alvarez, J. I., Charabati, M., Saint‐Laurent, O., Ghannam, S., Kébir, H., Flanagan, K., Yednock, T. A., Duquette, P., et al. (2015) · Annals of Neurology · doi:10.1002/ana.24415 · Cited by 80
Th17 cells in autoimmune diseases
Han, L., Yang, J. C., Wang, X., Li, D., Lv, L., & Li, B. (2015) · Frontiers of Medicine · doi:10.1007/s11684-015-0388-9 · Cited by 80
“Deficiency of granulocyte-macrophage colony-stimulating factor (GM-CSF) in autoreactive Th cells is resistant to the induction of EAE despite the presence of IL-17A or interferon (IFN)-γ [99].”
Background
Progress Toward the Elusive Pseudomonas aeruginosa Vaccine
Merakou, C., Schaefers, M., & Priebe, G. P. (2018) · Surgical Infections · doi:10.1089/sur.2018.233 · Cited by 68
CD4+ Tissue-resident Memory T Cells Expand and Are a Major Source of Mucosal Tumour Necrosis Factor α in Active Crohn’s Disease
Bishu, S., Zaatari, M. E., Hayashi, A., Hou, G., Bowers, N., Kinnucan, J. A. R., Manoogian, B., Muza–Moons, M. M., Zhang, M., Grasberger, H., et al. (2019) · Journal of Crohn s and Colitis · doi:10.1093/ecco-jcc/jjz010 · Cited by 76
Th17 cell pathogenicity in autoimmune disease
Park, E., & Ciofani, M. (2025) · Experimental & Molecular Medicine · doi:10.1038/s12276-025-01535-9 · Cited by 75
Foxo3 Transcription Factor Drives Pathogenic T Helper 1 Differentiation by Inducing the Expression of Eomes
Stienne, C., Michieletto, M. F., Benamar, M., Carrié, N., Bernard, I., Nguyen, X., Lippi, Y., Duguet, F., Liblau, R., Hedrick, S. Μ., et al. (2016) · Immunity · doi:10.1016/j.immuni.2016.09.010 · Cited by 71
“Both Th1 and Th17 cells can secrete GM-CSF during EAE (Codarri et al., 2011).”
Background
The IL-12 Cytokine and Receptor Family in Graft-vs.-Host Disease
Bastian, D. A., Wu, Y., Betts, B. C., & Yu, X. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.00988 · Cited by 75
Th17 reprogramming of T cells in systemic juvenile idiopathic arthritis
Henderson, L. A., Hoyt, K. J., Lee, P. Y., Rao, D. A., Jonsson, A. H., Nguyen, J. P., Rutherford, K. D., Julé, A. M., Charbonnier, L., Case, S., et al. (2020) · JCI Insight · doi:10.1172/jci.insight.132508 · Cited by 73
“joints of chronic sJIA patients compared with healthy control blood, including markers associated with pathogenic Th17 cells (CSF2, GM-CSF) (Figure 5F) (62, 63).”
Background
Physiological and pathophysiological functions of SOCE in the immune system
Patrick, J. S. (2011) · Frontiers in Bioscience-Elite · doi:10.2741/540 · Cited by 71
“It was recently found that granulocyte macrophage colony stimulating factor (GM-CSF) production by Th17 cells is required to induce EAE (49, 50).”
BackgroundInfluential
Human Adipose-Derived Mesenchymal Stem Cells Modulate Experimental Autoimmune Arthritis by Modifying Early Adaptive T Cell Responses
López‐Santalla, M., Mancheño‐Corvo, P., Menta, R., López-Belmonte, J. L., DelaRosa, O., Bueren, J. A., Dalemans, W., Lombardo, E., & Garin, M. I. (2015) · Stem Cells · doi:10.1002/stem.2113 · Cited by 73
Serum cytokines and anxiety in adolescent depression patients: Gender effect
Pallavi, P., Sagar, R., Mehta, M., Sharma, S., Subramanian, A., Shamshi, F., Sengupta, U., Pandey, R. M., & Mukhopadhyay, A. K. (2015) · Psychiatry Research · doi:10.1016/j.psychres.2015.06.036 · Cited by 69
Regulation of the neurodegenerative process associated to Parkinson's disease by CD4+ T-cells
González, H., Contreras, F., & Pacheco, R. (2015) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-015-9618-9 · Cited by 70
GM-CSF induces noninflammatory proliferation of microglia and disturbs electrical neuronal network rhythms in situ
Dikmen, H. O., Hemmerich, M., Lewen, A., Hollnagel, J., Chausse, B., & Kann, O. (2020) · Journal of Neuroinflammation · doi:10.1186/s12974-020-01903-4 · Cited by 69
“Microglia are the tissue-resident macrophages of the central nervous system (CNS) that become activated in most brain disorders, such as stroke, bacterial meningoencephalitis, multiple sclerosis, and Alzheimer’s disease [1, 2].”
Influential
Maintenance of Immune Homeostasis through ILC/T Cell Interactions
von Burg, N., Turchinovich, G., & Finke, D. (2015) · Frontiers in Immunology · doi:10.3389/fimmu.2015.00416 · Cited by 69
Soluble Factors Secreted by T Cells Promote β-Cell Proliferation
Dirice, E., Kahraman, S., Jiang, W., Ouaamari, A. E., Jesus, D. F. D., Teo, A. K. K., Hu, J. Y., Kawamori, D., Gaglia, J. L., Mathis, D. J., et al. (2013) · Diabetes · doi:10.2337/db13-0204 · Cited by 70
“factors such as GM-CSF (granulocyte macrophage-colony stimulating factor) (39) to influence leukocytes and recruit them to inflammatory sites during inflammation (40; 41).”
Background
The Enigmatic Role of Viruses in Multiple Sclerosis: Molecular Mimicry or Disturbed Immune Surveillance?
Geginat, J., Paroni, M., Pagani, M., Galimberti, D., Francesco, R. D., Scarpini, E. A., & Abrignani, S. (2017) · Trends in Immunology · doi:10.1016/j.it.2017.04.006 · Cited by 73
Lipid metabolism in Th17 cell function
Kanno, T., Nakajima, T., Miyako, K., & Endo, Y. (2023) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2023.108411 · Cited by 70
Cross‐talk between pathogen recognizing Toll‐like receptors and immunoglobulin Fc receptors in immunity
van Egmond, M., Vidarsson, G., & Bakema, J. E. (2015) · Immunological Reviews · doi:10.1111/imr.12333 · Cited by 69
“By contrast, TLR3 signaling (via TRIF) suppresses demyelination in EAE (86).”
Influential
Intravenous Gammaglobulin Inhibits Encephalitogenic Potential of Pathogenic T Cells and Interferes with their Trafficking to the Central Nervous System, Implicating Sphingosine-1 Phosphate Receptor 1–Mammalian Target of Rapamycin Axis
Othy, S., Hegde, P., Topçu, S., Sharma, M., Maddur, M. S., Lacroix‐Desmazes, S., Bayry, J., & Kaveri, S. V. (2013) · The Journal of Immunology · doi:10.4049/jimmunol.1201965 · Cited by 69
“Further, IVIg treatment decreased the expression of GM-CSF and podoplanin in FcgRIIB2/2 mice, rendering them less encephalitogenic (Fig.”
BackgroundInfluential
IFN-γ ameliorates autoimmune encephalomyelitis by limiting myelin lipid peroxidation
Sosa, R. A., Murphey, C. L., Robinson, R. R., & Forsthuber, T. G. (2015) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1505955112 · Cited by 70
“To test whether NAC treatment affected the frequencies or cytokine differentiation of MOG35–55–specific CD4+ T-cell responses, we performed cytokine ELISPOT assays for IFN-γ, IL-17, GM-CSF, and IL-5.”
BackgroundInfluential
Production of IL-17 by MAIT Cells Is Increased in Multiple Sclerosis and Is Associated with IL-7 Receptor Expression
Willing, A., Jäger, J., Reinhardt, S., Kursawe, N., & Friese, M. A. (2018) · The Journal of Immunology · doi:10.4049/jimmunol.1701213 · Cited by 70
“Moreover, MAIT cells are able to produce GM-CSF, another cytokine implicated in MS pathology (12, 51), and it has been shown for CD4 T cells that STAT-5 signaling after IL-7 or IL-2 exposure induces GM-CSF production (52, 53).”
Background
Pro-inflammatory T helper 17 directly harms oligodendrocytes in neuroinflammation
Larochelle, C., Wasser, B., Jamann, H., Löffel, J. T., Cui, Q., Tastet, O., Schillner, M., Luchtman, D. W., Birkenstock, J., Stroh, A., et al. (2021) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2025813118 · Cited by 72
“In particular, interleukin (IL)-23 – polarized T helper (Th)17 cells coexpressing T-bet and ROR-γ are considered pathogenic in both EAE (12, 13) and in MS (13 – 15).”
Nuclear Role of WASp in Gene Transcription Is Uncoupled from Its ARP2/3-Dependent Cytoplasmic Role in Actin Polymerization
Sadhukhan, S., Sarkar, K., Taylor, M. D., Candotti, F., & Vyas, Y. M. (2014) · The Journal of Immunology · doi:10.4049/jimmunol.1302923 · Cited by 67
“Such findings align with the previous report that showed an inverse correlation between TH1 cytokine expression and CSF2 activation (42).”
Result
STAT4 controls GM-CSF production by both Th1 and Th17 cells during EAE
McWilliams, I. L., Rajbhandari, R., Nozell, S. E., Benveniste, E. N., & Harrington, L. E. (2015) · Journal of Neuroinflammation · doi:10.1186/s12974-015-0351-3 · Cited by 73
“Recent reports have indicated that GM-CSF is critical for EAE induction and is produced by both Th1 and Th17 subsets [22, 23].”
BackgroundInfluential
IL‐12‐polarized Th1 cells produce GM‐CSF and induce EAE independent of IL‐23
Grifka‐Walk, H. M., Giles, D. A., & Segal, B. M. (2015) · European Journal of Immunology · doi:10.1002/eji.201545800 · Cited by 71
The Role of IL-15 in Activating STAT5 and Fine-Tuning IL-17A Production in CD4 T Lymphocytes
Pandiyan, P., Yang, X., Saravanamuthu, S. S., Zheng, L., Ishihara, S., O’Shea, J. J., & Lenardo, M. J. (2012) · The Journal of Immunology · doi:10.4049/jimmunol.1201476 · Cited by 69
Circulating Monocytes Are Reduced by Sphingosine-1-Phosphate Receptor Modulators Independently of S1P3
Lewis, N. D., Haxhinasto, S. A., Anderson, S. M., Stefanopoulos, D. E., Fogal, S. E., Adusumalli, P., Desai, S. N., Patnaude, L. A., Lukas, S., Ryan, K. R., et al. (2013) · The Journal of Immunology · doi:10.4049/jimmunol.1201810 · Cited by 69
“Pathogenesis in EAE models can be blocked by either reducing T cells (30) or monocytes, as illustrated by treating mice and rats with clodronate liposomes (31).”
Background
Brief Report: T Cell Expression of Granulocyte–Macrophage Colony‐Stimulating Factor in Juvenile Arthritis Is Contingent Upon Th17 Plasticity
Piper, C. J. M., Pesenacker, A. M., Bending, D., Thirugnanabalan, B., Varsani, H., Wedderburn, L. R., & Nistala, K. (2014) · Arthritis & Rheumatology · doi:10.1002/art.38647 · Cited by 68
“Although GM-CSF is widely expressed in both stromal and hematopoietic compartments, recent murine studies suggest that GM-CSF from the hematopoietic compartment, particularly CD4 T cells, is essential for disease (6,7,11).”
BackgroundResultInfluential
Astrocytes to the rescue! Glia limitans astrocytic endfeet control CNS inflammation
Quintana, F. J. (2017) · Journal of Clinical Investigation · doi:10.1172/jci95769 · Cited by 66
“For example, it would be interesting to study whether TNFα and GM-CSF, cytokines known to contribute to disease pathology in MS and other neurologic disorders (16, 17), can also induce tight junction formation at the glia limitans.”
Trim33 mediates the proinflammatory function of Th17 cells
Tanaka, S., Jiang, Y., Martínez, G., Tanaka, K., Yan, X. S., Kurosaki, T., Kaartinen, V., Feng, X., Tian, Q., Wang, X., et al. (2018) · The Journal of Experimental Medicine · doi:10.1084/jem.20170779 · Cited by 73
“GM-CSF produced by Th1 and Th17 cells was shown to play an essential role in EAE (Codarri et al., 2011; El-Behi et al., 2011).”
Background
IL-17 Silencing Does Not Protect Nonobese Diabetic Mice from Autoimmune Diabetes
Joseph, J., Bittner, S., Kaiser, F. M. P., Wiendl, H., & Kissler, S. (2011) · The Journal of Immunology · doi:10.4049/jimmunol.1101215 · Cited by 68
“Furthermore, the pathogenicity of Th17 cells in EAE was very recently shown to critically depend on their secretion of GM-CSF (26, 27).”
Background
Activated leukocyte cell adhesion molecule regulates B lymphocyte migration across central nervous system barriers
Michel, L., Grasmuck, C., Charabati, M., Lécuyer, M., Zandee, S., Dhaeze, T., Alvarez, J. I., Li, R., Larouche, S., Bourbonnière, L., et al. (2019) · Science Translational Medicine · doi:10.1126/scitranslmed.aaw0475 · Cited by 72
The CNS mononuclear phagocyte system in health and disease
Mundt, S., Greter, M., & Becher, B. (2022) · Neuron · doi:10.1016/j.neuron.2022.10.005 · Cited by 68
New candidates for CD4 T cell pathogenicity in experimental neuroinflammation and multiple sclerosis
Hoppmann, N., Graetz, C., Paterka, M., Poisa-Beiro, L., Larochelle, C., Hasan, M., Lill, C. M., Zipp, F., & Siffrin, V. (2015) · Brain · doi:10.1093/brain/awu408 · Cited by 66
“These recent publications underline the importance of GM-CSF producing T cells in multiple sclerosis for T cell pathogenicity, which had been suggested by recent work in EAE (Codarri et al., 2011; El-Behi et al., 2011).”
Background
Structure-based design of substituted hexafluoroisopropanol-arylsulfonamides as modulators of RORc
Fauber, B. P., Boenig, G. D. L., Burton, B., Eidenschenk, C., Everett, C., Gobbi, A., Hymowitz, S. G., Johnson, A. R., Liimatta, M. B., Lockey, P. M., et al. (2013) · Bioorganic & Medicinal Chemistry Letters · doi:10.1016/j.bmcl.2013.10.054 · Cited by 66
The Emerging Roles of Gamma–Delta T Cells in Tissue Inflammation in Experimental Autoimmune Encephalomyelitis
Malik, S., Want, M. Y., & Awasthi, A. (2016) · Frontiers in Immunology · doi:10.3389/fimmu.2016.00014 · Cited by 68
GM-CSF as a therapeutic target in autoimmune diseases
Shiomi, A., Usui, T., & Mimori, T. (2016) · Inflammation and Regeneration · doi:10.1186/s41232-016-0014-5 · Cited by 69
“Ectopic RORγt expression showed that RORγt drove GM-CSF production in Th cells [4].”
BackgroundResultInfluential
GM-CSF promotes chronic disability in EAE by altering the composition of CNS myeloid cells, but is dispensable for disease induction
Duncker, P., Stoolman, J., Huber, A. K., & Segal, B. (2017) · Journal of Immunology · doi:10.4049/jimmunol.1701484 · Cited by 48
“of EAE in otherwise immunocompetent C57BL/6 mice is dependent on GM-CSF expression during the effector phase (8, 9).”
Background
Pharmacological inhibition of RORγt suppresses the Th17 pathway and alleviates arthritis in vivo
Guendisch, U., Weiss, J., Ecoeur, F., Riker, J., Kaupmann, K., Kallen, J., Hintermann, S., Orain, D., Dawson, J., Billich, A., et al. (2017) · PLoS ONE · doi:10.1371/journal.pone.0188391 · Cited by 62
Differentiation of Pathogenic Th17 Cells Is Negatively Regulated by Let-7 MicroRNAs in a Mouse Model of Multiple Sclerosis
Angelou, C. C., Wells, A. C., Vijayaraghavan, J., Dougan, C. E., Lawlor, R. G., Iverson, E., Lazarevic, V., Kimura, M. Y., Peyton, S. R., Minter, L. M., et al. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2019.03125 · Cited by 63
The Ins and Outs of Central Nervous System Inflammation—Lessons Learned from Multiple Sclerosis
Ramaglia, V., Rojas, O. L., Naouar, I., & Gommerman, J. L. (2021) · Annual Review of Immunology · doi:10.1146/annurev-immunol-093019-124155 · Cited by 72
Targeting GM-CSF in inflammatory and autoimmune disorders
Achuthan, A. A., Lee, M.-C., & Hamilton, J. A. (2021) · Seminars in Immunology · doi:10.1016/j.smim.2021.101523 · Cited by 66
Differential roles of resident microglia and infiltrating monocytes in murine CNS autoimmunity
Shemer, A., & Jung, S. (2015) · Seminars in Immunopathology · doi:10.1007/s00281-015-0519-z · Cited by 66
“Interestingly, most of these cytokines could be ruled out as being required for EAE development, while GM-CSF appeared to be critical [103].”
Allergies – A T cells perspective in the era beyond the TH1/TH2 paradigm
Berker, M., Frank, L. J., Geßner, A. L., Graßl, N., Holtermann, A., Höppner, S., Kraef, C., Leclaire, M. D., Maier, P., Messerer, D. A. C., et al. (2016) · Clinical Immunology · doi:10.1016/j.clim.2016.11.001 · Cited by 67
CD70 defines a subset of proinflammatory and CNS-pathogenic TH1/TH17 lymphocytes and is overexpressed in multiple sclerosis
Dhaeze, T., Tremblay, L., Lachance, C., Peelen, E., Zandee, S., Grasmuck, C., Bourbonnière, L., Larouche, S., Ayrignac, X., Rébillard, R., et al. (2019) · Cellular and Molecular Immunology · doi:10.1038/s41423-018-0198-5 · Cited by 63
Astrocytes in multiple sclerosis and experimental autoimmune encephalomyelitis: Star-shaped cells illuminating the darkness of CNS autoimmunity
Yi, W., Schlüter, D., & Wang, X. (2019) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2019.05.029 · Cited by 67
Gut dysbiosis and multiple sclerosis
Noto, D., & Miyake, S. (2020) · Clinical Immunology · doi:10.1016/j.clim.2020.108380 · Cited by 65
The neuroimmune connectome in health and disease
Wheeler, M. A., & Quintana, F. J. (2025) · Nature · doi:10.1038/s41586-024-08474-x · Cited by 71
“Inter-estingly, CXCR4 + T H 17 cells have also been described to contribute to MS pathogenesis 30,31 .”
Increased inflammasome related gene expression profile in PBMC may facilitate T helper 17 cell induction in multiple sclerosis.
Peelen, E., Damoiseaux, J., Muris, A., Knippenberg, S., Smolders, J., Hupperts, R., & Thewissen, M. (2015) · Molecular Immunology · doi:10.1016/j.molimm.2014.10.008 · Cited by 66
Fatal Eosinophilic Myocarditis Develops in the Absence of IFN-γ and IL-17A
Barin, J. G., Baldeviano, G. C., Talor, M. V., Wu, L., Ong, S., Fairweather, D., Bedja, D., Stickel, N., Fontes, J. A., Cardamone, A., et al. (2013) · The Journal of Immunology · doi:10.4049/jimmunol.1301282 · Cited by 66
“IFN-gIL-17A mice were not protected from EAE, nor did they develop accelerated disease (73).”
Background
Discovery of 1-{4-[3-Fluoro-4-((3 S ,6 R )-3-methyl-1,1-dioxo-6-phenyl-[1,2]thiazinan-2-ylmethyl)-phenyl]-piperazin-1-yl}-ethanone (GNE-3500): a Potent, Selective, and Orally Bioavailable Retinoic Acid Receptor-Related Orphan Receptor C (RORc or RORγ) Inverse Agonist
Fauber, B. P., René, O., Deng, Y., DeVoss, J., Eidenschenk, C., Everett, C., Ganguli, A., Gobbi, A., Hawkins, J., Johnson, A. R., et al. (2015) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.5b00597 · Cited by 65
GM-CSF but Not IL-17 Is Critical for the Development of Severe Interstitial Lung Disease in SKG Mice
Shiomi, A., Usui, T., Ishikawa, Y., Shimizu, M., Murakami, K., & Mimori, T. (2014) · The Journal of Immunology · doi:10.4049/jimmunol.1303255 · Cited by 65
“Recent reports demonstrated that not IL-17A, but GM-CSF was critical for the pathogenesis of Th cells in experimental autoimmune encephalomyelitis, which had been known as a Th17-mediated disease (19, 20).”
Background
Liver fibrosis and CD206+ macrophage accumulation are suppressed by anti-GM-CSF therapy
Tan-Garcia, A., Lai, F., Yeong, J. P.-S., Irac, S. E., Ng, P. Y., Msallam, R., Lim, J. C. T., Wai, L., Tham, C. Y. L., Choo, S. P., et al. (2019) · JHEP Reports · doi:10.1016/j.jhepr.2019.11.006 · Cited by 63
“For cell surface phenotyping related to in vitro and in vivo GM-CSF blocking experiments, the following antibodies were used: CD3-BV650 (SP34-2), CD5-BV711 (UCHT2), CD14-PE/Cy7 (M5E2), CD14-AF700 (M5E2), CD19-BV650 (SJ25C1), CD20-BV650 (2H7), CD45-V500 (HI30), CD45RA-FITC (5H9), CD123-BUV395 (7G3), CD169-PE (7-239), C…”
Influential
The development of LTi cells
Cherrier, M., & Eberl, G. (2012) · Current Opinion in Immunology · doi:10.1016/j.coi.2012.02.003 · Cited by 63
“Other cytokines produced by Th17 cells include IL-22, which also activates epithelial cells to produce anti-microbial peptides, and GM-CSF, which induces a positive feedback loop on the differentiation of Th17 cells and the recruitment of myeloid cells [16,17].”
Background
Immunopathogenesis of Neuromyelitis Optica
Levy, M., Wildemann, B., Jarius, S., Arellano, B., Sasidharan, S., Weber, M. S., & Stüve, O. (2014) · Advances in immunology · doi:10.1016/b978-0-12-800100-4.00006-4 · Cited by 61
Innate Immunity Cells and the Neurovascular Unit
Presta, I., Vismara, M. F. M., Novellino, F., Donato, A., Zaffino, P., Scali, E., Pirrone, K. C., Spadea, M. F., Malara, N., & Donato, G. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19123856 · Cited by 61
GM-CSF: Master regulator of the T cell-phagocyte interface during inflammation
Ingelfinger, F., De Feo, D., & Becher, B. (2021) · Seminars in Immunology · doi:10.1016/j.smim.2021.101518 · Cited by 61
Neutrophil Homeostasis and Emergency Granulopoiesis: The Example of Systemic Juvenile Idiopathic Arthritis
Malengier‐Devlies, B., Metzemaekers, M., Wouters, C. H., Proost, P., & Matthys, P. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.766620 · Cited by 64
Cytokine control of inflammation and repair in the pathology of multiple sclerosis.
Rodgers, J. M., & Miller, S. D. (2012) · Europe PMC (PubMed Central) · Cited by 60
Advances in T Helper 17 Cell Biology: Pathogenic Role and Potential Therapy in Multiple Sclerosis
Volpe, E., Battistini, L., & Borsellino, G. (2015) · Mediators of Inflammation · doi:10.1155/2015/475158 · Cited by 64
Immunoregulatory effect of mast cells influenced by microbes in neurodegenerative diseases
Girolamo, F., Coppola, C., & Ribatti, D. (2017) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2017.06.017 · Cited by 61
Impact of aging immune system on neurodegeneration and potential immunotherapies
Liang, Z., Zhao, Y., Ruan, L., Zhu, L., Jin, K., Zhuge, Q., Su, D., & Zhao, Y. L. (2017) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2017.07.006 · Cited by 64
“Although the etiology is not fully understood, inflammaging has been attributed to a combination of cellular senescence-induced SASP that releases low levels of pro-inflammatory cytokines, such as IL-6, TNF-a, IL-1b, and CRP (Campisi, 2011; Freund et al., 2010; Olivieri et al., 2013, 2012), and the persistent activati…”
Influential
A T cell-specific deletion of HDAC1 protects against experimental autoimmune encephalomyelitis
Göschl, L., Preglej, T., Hamminger, P., Bonelli, M. M., Andersen, L., Boucheron, N., Gülich, A. F., Müller, L., Saferding, V., Mufazalov, I. A., et al. (2017) · Journal of Autoimmunity · doi:10.1016/j.jaut.2017.09.008 · Cited by 62
Paving the way towards an effective treatment for multiple sclerosis: advances in cell therapy
Mansilla, M. J., Presas‐Rodríguez, S., Teniente‐Serra, A., González-Larreategui, Í., Quirant‐Sánchez, B., Fondelli, F., Djedović, N., Iwaszkiewicz‐Grześ, D., Chwojnicki, K., Miljković, D. M., et al. (2021) · Cellular and Molecular Immunology · doi:10.1038/s41423-020-00618-z · Cited by 64
Modulation of autoimmune diseases by interleukin (IL)-17 producing regulatory T helper (Th17) cells.
Singh, B., Schwartz, J. A., Sandrock, C., Bellemore, S. M., & Nikoopour, E. (2013) · Europe PMC (PubMed Central) · Cited by 59
Selective ORAI1 Inhibition Ameliorates Autoimmune Central Nervous System Inflammation by Suppressing Effector but Not Regulatory T Cell Function
Kaufmann, U., Shaw, P. J., Kozhaya, L., Subramanian, R., Gaida, K., Unutmaz, D., McBride, H. J., & Feske, S. (2015) · The Journal of Immunology · doi:10.4049/jimmunol.1501406 · Cited by 61
“Although GM-CSF is induced by RORgt and IL-23, both pathogenic subsets of Th1 and Th17 cells express GM-CSF in vivo (10).”
Background
Sustained TNF production by central nervous system infiltrating macrophages promotes progressive autoimmune encephalomyelitis
Valentin-Torres, A., Savarin, C., Hinton, D. R., Phares, T. W., Bergmann, C. C., & Stohlman, S. A. (2016) · Journal of Neuroinflammation · doi:10.1186/s12974-016-0513-y · Cited by 63

Authors: Codarri, L., Gyülvészi, G., Tosevski, V., Hesske, L., Fontana, A., Magnenat, L., Suter, T., & Becher, B.
Affiliations: University Hospital Zurich (CH)
University of Zurich (CH)
Merck Serono S.A. (Switzerland) (CH)
Corresponding author: Becher, Burkhard
ORCID: Magnenat, Laurent
Suter, Tobias
Becher, Burkhard
Venue: Nature Immunology
Publisher: Springer Science and Business Media LLC
Published: 2011-04-24
Volume: 12
Issue: 6
Pages: 560-567
ISSN: 1529-2908 (ISSN-L)
1529-2916
DOI: 10.1038/ni.2027
OpenAlex: W2157837362
Cited by: 1,191
References: 44
Citations by year: 2026: 31 · 2025: 48 · 2024: 60 · 2023: 53 · 2022: 61 · 2021: 73 · 2020: 85 · 2019: 83 · 2018: 72 · 2017: 99 · 2016: 96 · 2015: 117 · 2014: 103 · 2013: 98 · 2012: 82
FWCI: 70.23
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature Immunology (publishedVersion)
PubMed (publishedVersion)
Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
Topics: Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords: RORγt, GM-CSF, experimental autoimmune encephalomyelitis, T helper cells, IL-23, autoimmune neuroinflammation, Th1 cells, Th17 cells, myeloid cell infiltration, IL-12, interferon-gamma, IL-27, cytokine regulation
MeSH terms: Animals, Cells, Cultured, Encephalomyelitis, Autoimmune, Experimental, Female, Flow Cytometry, Glycoproteins, T-Lymphocytes, Helper-Inducer, Interferon-gamma, Interleukins, Male, Mice, Inbred C57BL, Mice, Inbred Strains, Mice, Transgenic, Peptide Fragments, Granulocyte-Macrophage Colony-Stimulating Factor, Mice, Knockout, Th1 Cells, Interleukin-12, Interleukin-17, Mice, Interleukin-23, Nuclear Receptor Subfamily 1, Group F, Member 3, Th17 Cells, Myelin-Oligodendrocyte Glycoprotein

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

RORγt drives production of the cytokine GM-CSF in helper T cells, which is essential for the effector phase of autoimmune neuroinflammation

Abstract

Overview

Integrity signals

Verification

Claims the paper makes

Claims other papers make about this one

Citations

Cites

Cited by

Related

Metadata

Record

About these checks