[1]
|
McInnes, I.B., Asahina, A., Coates, L.C., et al. (2023) Bimekizumab in Patients with Psoriatic Arthritis, Naive to Bio-logic Treatment: A Randomised, Double-Blind, Placebo-Controlled, Phase 3 Trial (BE OPTIMAL). The Lancet, 401, 25-37. https://doi.org/10.1016/S0140-6736(22)02302-9
|
[2]
|
Sun, N., Guo, H. and Wang, Y. (2019) Retinoic Acid Receptor-Related Orphan Receptor γ-t (RORγt) Inhibitors in Clinical Development for the Treatment of Autoimmune Diseases. Expert Opinion on Therapeutic Patents, 29, 663-674. https://doi.org/10.1080/13543776.2019.1655541
|
[3]
|
Chaparro, M., Garre, A., Iborra, M., et al. (2021) Effective-ness and Safety of Ustekinumab in Ulcerative Colitis: Real-World Evidence from the ENEIDA Registry. Journal of Crohn’s and Colitis, 15, 1846-1851.
|
[4]
|
Moreau, J.M., Velegraki, M., Bolyard, C., Rosenblum, M.D. and Li, Z.H. (2022) Transforming Growth Factor-β1 in Regulatory T Cell Biology. Science Immunology, 7, eabi4613. https://doi.org/10.1126/sciimmunol.abi4613
|
[5]
|
Xu, H., Wu, L., Nguyen, H.H., et al. (2021) Arkadia-SKI/SnoN Signaling Differentially Regulates TGF-β—Induced iTreg and Th17 Cell Differentiation. Journal of Experimental Medi-cine, 218, e20210777.
https://doi.org/10.1084/jem.20210777
|
[6]
|
Su, J., Morgani, S.M., David, C.J., et al. (2020) TGF-β Orchestrates Fibrogenic and Developmental EMTs via the RAS Effector RREB1. Nature, 577, 566-571. https://doi.org/10.1038/s41586-019-1897-5
|
[7]
|
Liu, Y., Song, J., Yang, J., et al. (2021) Tumor Necrosis Factor α-Induced Protein 8-Like 2 Alleviates Nonalcoholic Fatty Liver Disease through Suppressing Transforming Growth Factor β-Activated Kinase 1 Activation. Hepatology, 74, 1300-1318. https://doi.org/10.1002/hep.31832
|
[8]
|
Zhao, H.Y., Zhang, Y.Y., Xing, T., et al. (2021) M2 Macrophages, But Not M1 Macrophages, Support Megakaryopoiesis by Upregulating PI3K-AKT Pathway Activity. Signal Transduction and Targeted Therapy, 6, Article No. 234.
https://doi.org/10.1038/s41392-021-00627-y
|
[9]
|
Sobierajska, K., Wawro, M.E. and Niewiarowska, J. (2022) Oxidative Stress Enhances the TGF-β2-RhoA-MRTF-A/B Axis in Cells Entering Endothelial-Mesenchymal Transition. International Journal of Molecular Science, 23, Article 2062. https://doi.org/10.3390/ijms23042062
|
[10]
|
Batlle, E. and Massagué, J. (2019) Transforming Growth Factor-β Signaling in Immunity and Cancer. Immunity, 50, 924-940. https://doi.org/10.1016/j.immuni.2019.03.024
|
[11]
|
Yoon, J.H., Sudo, K., Kuroda, M., et al. (2015) Phosphoryla-tion Status Determines the Opposing Functions of Smad2/Smad3 as STAT3 Cofactors in TH17 Differentiation. Nature Communications, 6, Article No. 7600.
https://doi.org/10.1038/ncomms8600
|
[12]
|
Martinez, G.J., Zhang, Z., Reynolds, J.M., et al. (2010) Smad2 Posi-tively Regulates the Generation of Th17 Cells. Journal of Biological Chemistry, 285, 29039-29043. https://doi.org/10.1074/jbc.C110.155820
|
[13]
|
Martinez, G.J., Zhang, Z., Chung, Y., et al. (2009) Smad3 Differen-tially Regulates the Induction of Regulatory and Inflammatory T Cell Differentiation. Journal of Biological Chemistry, 284, 35283-35286.
https://doi.org/10.1074/jbc.C109.078238
|
[14]
|
Xu, Q., Jin, X., Zheng, M., et al. (2019) Phosphatase PP2A Is Es-sential for TH17 Differentiation. Proceedings of the National Academy of Sciences of the United States of America, 116, 982-987. https://doi.org/10.1073/pnas.1807484116
|
[15]
|
Malhotra, N., Robertson, E. and Kang, J. (2010) Smad2 Is Essential for TGF β-Mediated Th17 Cell Generation. Journal of Biological Chemistry, 285, 29044-29048. https://doi.org/10.1074/jbc.C110.156745
|
[16]
|
Wang, F., Yang, Y., Li, Z., et al. (2022) Mannan-Binding Lectin Regulates the Th17/Treg Axis through JAK/STAT and TGF-β/SMAD Signaling against Candida albicans Infection. Journal of Inflammation Research, 15, 1797-1810. https://doi.org/10.2147/JIR.S344489
|
[17]
|
Chitrakar, A., Budda, S.A., Henderson, J.G., Axtell, R.C. and Zenewicz, L.A. (2020) E3 Ubiquitin Ligase Von Hippel-Lindau Protein Pro-motes Th17 Differentiation. Journal of Immunology, 205, 1009-1023.
https://doi.org/10.4049/jimmunol.2000243
|
[18]
|
Corral-Jara, K.F., Chauvin, C., Abou-Jaoudé, W., et al. (2021) In-terplay between SMAD2 and STAT5A Is a Critical Determinant of IL-17A/IL-17F Differential Expression. Molecular Biomedicine, 2, Article No. 9.
https://doi.org/10.1186/s43556-021-00034-3
|
[19]
|
Rus, V., Nguyen, V., Tatomir, A., et al. (2017) RGC-32 Pro-motes Th17 Cell Differentiation and Enhances Experimental Autoimmune Encephalomyelitis. Journal of Immunology, 198, 3869-3877.
https://doi.org/10.4049/jimmunol.1602158
|
[20]
|
Prado, D.S., Cattley, R.T., Shipman, C.W., et al. (2021) Synergis-tic and Additive Interactions between Receptor Signaling Networks Drive the Regulatory T Cell versus T Helper 17 Cell Fate Choice. Journal of Biological Chemistry, 297, Article 101330. https://doi.org/10.1016/j.jbc.2021.101330
|
[21]
|
Kurisaki, A., Kose, S., Yoneda, Y., Heldin, C.H. and Moustakas, A. (2001) Transforming Growth Factor-β Induces Nuclear Import of Smad3 in an Importin-β1 and Ran-Dependent Manner. Molecular Biology of the Cell, 12, 1079-1091. https://doi.org/10.1091/mbc.12.4.1079
|
[22]
|
Lo, R.S., Chen, Y.G., Shi, Y., Pavletich, N.P. and Massagué, J. (1998) The L3 Loop: A Structural Motif Determining Specific Interactions between Smad Proteins and TGF-β Receptors. The EMBO Journal, 17, 996-1005.
https://doi.org/10.1093/emboj/17.4.996
|
[23]
|
Kawasaki, N., Miwa, T., Hokari, S., et al. (2018) Long Noncoding RNA NORAD Regulates Transforming Growth Factor-β Signaling and Epithelial-to-Mesenchymal Transition-Like Phenotype. Cancer Science, 109, 2211-2220.
https://doi.org/10.1111/cas.13626
|
[24]
|
Lees, C.W., Barrett, J.C., Parkes, M. and Satsangi, J. (2011) New IBD Ge-netics: Common Pathways with Other Diseases. Gut, 60, 1739-1753. https://doi.org/10.1136/gut.2009.199679
|
[25]
|
Ntunzwenimana, J.C., Boucher, G., Paquette, J., et al. (2021) Func-tional Screen of Inflammatory Bowel Disease Genes Reveals Key Epithelial Functions. Genome Medicine, 13, Article No. 181. https://doi.org/10.1101/2021.10.15.464566
|
[26]
|
Abraham, C., Dulai, P.S., Vermeire, S. and Sandborn, W.J. (2017) Lessons Learned from Trials Targeting Cytokine Pathways in Patients with Inflammatory Bowel Diseases. Gas-troenterology, 152, 374-388.E4.
https://doi.org/10.1053/j.gastro.2016.10.018
|
[27]
|
Fiocchi, C. (2001) TGF-β/Smad Signaling Defects in Inflamma-tory Bowel Disease: Mechanisms and Possible Novel Therapies for Chronic Inflammation. Journal of Clinical Investiga-tion, 108, 523-526. https://doi.org/10.1172/JCI13863
|
[28]
|
Paik, J., Meeker, S., Hsu, C.C., et al. (2020) Validation Studies for Germ-Free Smad3-/- Mice as a Bio-Assay to Test the Causative Role of Fecal Microbiomes in IBD. Gut Mi-crobes, 11, 21-31.
https://doi.org/10.1080/19490976.2019.1611151
|
[29]
|
Coskun, M., Vermeire, S. and Nielsen, O.H. (2017) Novel Targeted Therapies for Inflammatory Bowel Disease. Trends in Pharmacological Sciences, 38, 127-142. https://doi.org/10.1016/j.tips.2016.10.014
|
[30]
|
Yang, M., Zhu, X., Fu, F., et al. (2022) Baicalin Ameliorates In-flammatory Response in a Mouse Model of Rhinosinusitis via Regulating the Treg/Th17 Balance. Ear, Nose & Throat Journal, 101, 8S-16S.
https://doi.org/10.1177/0145561320986058
|
[31]
|
Li, Z., Gu, J., Zhu, Q., et al. (2017) Obese Donor Mice Spleno-cytes Aggravated the Pathogenesis of Acute Graft-versus-Host Disease via Regulating Differentiation of Tregs and CD4+ T Cell Induced-Type I Inflammation. Oncotarget, 8, 74880-74896. https://doi.org/10.18632/oncotarget.20425
|
[32]
|
Aubart, M., Gobert, D., Aubart-Cohen, F., et al. (2014) Ear-ly-Onset Osteoarthritis, Charcot-Marie-Tooth Like Neuropathy, Autoimmune Features, Multiple Arterial Aneurysms and Dissections: An Unrecognized and Life Threatening Condition. PLOS ONE, 9, e96387. https://doi.org/10.1371/journal.pone.0096387
|
[33]
|
Zhang, M., Zhou, L., Xu, Y., et al. (2020) A STAT3 Pal-mitoylation Cycle Promotes Th17 Differentiation and Colitis. Nature, 586, 434-439. https://doi.org/10.1038/s41586-020-2799-2
|
[34]
|
Guanizo, A.C., Fernando, C.D., Garama, D.J. and Gough, D.J. (2018) STAT3: A Multifaceted Oncoprotein. Growth Factors, 36, 1-14. https://doi.org/10.1080/08977194.2018.1473393
|
[35]
|
Damasceno, L.E.A., Prado, D.S., Veras, F.P., et al. (2020) PKM2 Promotes Th17 Cell Differentiation and Autoimmune Inflammation by Fine-Tuning STAT3 Activation. Journal of Experimental Medicine, 217, e20190613.
https://doi.org/10.1084/jem.20190613
|
[36]
|
Nanduri, R., Mahajan, S., Bhagyaraj, E., et al. (2015) The Active Form of Vitamin D Transcriptionally Represses Smad7 Signaling and Activates Extracellular Signal-Regulated Kinase (ERK) to Inhibit the Differentiation of a Inflammatory T Helper Cell Subset and Suppress Experimental Autoimmune Encephalo-myelitis. Journal of Biological Chemistry, 290, 12222-12236. https://doi.org/10.1074/jbc.M114.621839
|
[37]
|
Delgoffe, G.M., Kole, T.P., Zheng, Y., et al. (2009) The mTOR Ki-nase Differentially Regulates Effector and Regulatory T Cell Lineage Commitment. Immunity, 30, 832-844. https://doi.org/10.1016/j.immuni.2009.04.014
|
[38]
|
Buttrick, T., Khoury, S.J. and Elyaman, W. (2020) Opposite Functions of STAT3 and Smad3 in Regulating Tiam1 Expression in Th17 Cells. Small GTPases, 11, 62-68. https://doi.org/10.1080/21541248.2017.1341365
|
[39]
|
Kaminski, S., Hermann-Kleiter, N., Meisel, M., et al. (2011) Coronin 1A Is an Essential Regulator of the TGFβ Receptor/SMAD3 Signaling Pathway in Th17 Cells. Journal of Au-toimmunity, 37, 198-208.
https://doi.org/10.1016/j.jaut.2011.05.018
|
[40]
|
Soukou, S., Huber, S. and Krebs, C.F. (2021) T Cell Plasticity in Renal Autoimmune Disease. Cell and Tissue Research, 385, 323-333. https://doi.org/10.1007/s00441-021-03466-z
|
[41]
|
Kotake, S., Yago, T., Kobashigawa, T. and Nanke, Y. (2017) The Plasticity of Th17 Cells in the Pathogenesis of Rheumatoid Arthritis. Journal of Clinical Medicine, 6, Article 67. https://doi.org/10.3390/jcm6070067
|
[42]
|
Gagliani, N., Amezcua Vesely, M.C., Iseppon, A., et al. (2015) Th17 Cells Transdifferentiate into Regulatory T Cells during Resolution of Inflammation. Nature, 523, 221-225. https://doi.org/10.1038/nature14452
|
[43]
|
Yang, P., Qian, F.Y., Zhang, M.F., et al. (2019) Th17 Cell Pathogenicity and Plasticity in Rheumatoid Arthritis. Journal of Leukocyte Biology, 106, 1233-1240. https://doi.org/10.1002/JLB.4RU0619-197R
|
[44]
|
Mills, K.H.G. (2023) IL-17 and IL-17-Producing Cells in Pro-tection versus Pathology. Nature Reviews Immunology, 23, 38-54. https://doi.org/10.1038/s41577-022-00746-9
|
[45]
|
Konieczny, P., Xing, Y., Sidhu, I., et al. (2022) Interleukin-17 Governs Hypoxic Adaptation of Injured Epithelium. Science, 377, eabg9302. https://doi.org/10.1126/science.abg9302
|
[46]
|
Hueber, W., Sands, B.E., Lewitzky, S., et al. (2012) Secukinumab, a Human Anti-IL-17A Monoclonal Antibody, for Moderate to Severe Crohn’s Disease: Unexpected Results of a Random-ised, Double-Blind Placebo-Controlled Trial. Gut, 61, 1693-1700. https://doi.org/10.1136/gutjnl-2011-301668
|
[47]
|
Ueno, A., Jeffery, L., Kobayashi, T., et al. (2018) Th17 Plasticity and Its Relevance to Inflammatory Bowel Disease. Journal of Autoimmunity, 87, 38-49. https://doi.org/10.1016/j.jaut.2017.12.004
|
[48]
|
Krebs, C.F. and Panzer, U. (2018) Plasticity and Heterogeneity of Th17 in Immune-Mediated Kidney Diseases. Journal of Autoimmunity, 87, 61-68. https://doi.org/10.1016/j.jaut.2017.12.005
|
[49]
|
Xu, H., Agalioti, T., Zhao, J., et al. (2020) The Induction and Func-tion of the Anti-Inflammatory Fate of Th17 Cells. Nature Communications, 11, Article No. 3334. https://doi.org/10.1038/s41467-020-17097-5
|
[50]
|
O’Donoghue, R.J., Knight, D.A., Richards, C.D., et al. (2012) Genetic Partitioning of Interleukin-6 Signalling in Mice Dissociates Stat3 from Smad3-Mediated Lung Fibrosis. EMBO Molecular Medicine, 4, 939-951.
https://doi.org/10.1002/emmm.201100604
|
[51]
|
Wang, G., Yu, Y., Sun, C., et al. (2016) STAT3 Selectively Inter-acts with Smad3 to Antagonize TGF-β Signalling. Oncogene, 35, 4388-4398. https://doi.org/10.1038/onc.2015.446
|
[52]
|
Itoh, Y., Saitoh, M. and Miyazawa, K. (2018) Smad3-STAT3 Crosstalk in Pathophysiological Contexts. Acta Biochimica et Biophysica Sinica, 50, 82-90. https://doi.org/10.1093/abbs/gmx118
|
[53]
|
Katsanos, K.H. and Papadakis, K.A. (2017) Inflammatory Bowel Dis-ease: Updates on Molecular Targets for Biologics. Gut Liver, 11, 455-463. https://doi.org/10.5009/gnl16308
|
[54]
|
Luo, K. (2017) Signaling cross Talk between TGF-β/Smad and Other Sig-naling Pathways. Cold Spring Harbor Perspectives in Biology, 9, a022137. https://doi.org/10.1101/cshperspect.a022137
|
[55]
|
Ooshima, A., Park, J. and Kim, S.J. (2019) Phosphorylation Status at Smad3 Linker Region Modulates Transforming Growth Factor-β-Induced Epithelial-Mesenchymal Transition and Cancer Progression. Cancer Science, 110, 481-488.
https://doi.org/10.1111/cas.13922
|
[56]
|
Liu, F. (2006) Smad3 Phosphorylation by Cyclin-Dependent Kinases. Cyto-kine & Growth Factor Reviews, 17, 9-17.
https://doi.org/10.1016/j.cytogfr.2005.09.010
|
[57]
|
Tarasewicz, E. and Jeruss, J.S. (2012) Phospho-Specific Smad3 Signaling: Impact on Breast Oncogenesis. Cell Cycle, 11, 2443-2451. https://doi.org/10.4161/cc.20546
|
[58]
|
Buxton, I.L. and Duan, D. (2008) Cyclic GMP/Protein Kinase G Phosphorylation of Smad3 Blocks Transforming Growth Fac-tor-β-Induced Nuclear Smad Translocation: A Key Antifibrogenic Mechanism of Atrial Natriuretic Peptide. Circulation Research, 102, 151-153. https://doi.org/10.1161/CIRCRESAHA.107.170217
|