Cited by 88

The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

Arid5a regulates naive CD4+ T cell fate through selective stabilization of Stat3 mRNA

Masuda, Kazuya, Ripley, Barry, Nyati, Kishan Kumar, Dubey, Praveen Kumar, Zaman, Mohammad Mahabub-Uz, Hanieh, Hamza, Higa, Mitsuru, Yamashita, Kazuo, Standley, Daron M., Mashima, Tsukasa, Katahira, Masato, Okamoto, Toru, Matsuura, Yoshiharu, Takeuchi, Osamu, Kishimoto, Tadamitsu·2016·Journal of Experimental Medicine

Abstract

Balance in signal transducer and activator of transcription (STAT) activation is a key factor in regulating the fate of naive CD4+ T cells. Here, we demonstrate that AT-rich interactive domain-containing protein 5a (Arid5a) in T cells directs naive CD4+ T cells to differentiate into inflammatory CD4+ T cells, especially Th17 cells, through selective stabilization of Stat3 (but not Stat1 and Stat5) mRNA in an IL-6–dependent manner. Loss of Arid5a in T cells led to reduction of STAT3 level under Th17-polarizing conditions, whereas STAT1 and STAT5 in Arid5a-deficient T cells were highly activated compared with those of WT T cells under the same conditions. These cells displayed the feature of antiinflammatory (Il10-expressing) CD4+ T cells. Thus, we show a T cell–intrinsic role of Arid5a on fate decisions of naive CD4+ T cells through selective stabilization of Stat3 mRNA.

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.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1084/jem.20151289

Cites

5 of 5 references verified0 citation errors · 0 not checkable

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.

A few free checks a day · papers already verified open instantly · results are public

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?

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

Flagged first, then by citations

Show all 5 references

Research works printed but not linked: 45

  1. Awasthi, 2007, A dominant function for interleukin 27 in generating interleukin 10-producing anti-inflammatory T cells, Nat. Immunol., 8, 1380, 10.1038/ni1541 · DOI · Paper page
  2. Bellaousov, 2013, RNAstructure: Web servers for RNA secondary structure prediction and analysis, Nucleic Acids Res., 41, W471–W474, 10.1093/nar/gkt290 · DOI
  3. Bromberg, 1999, Stat3 as an oncogene, Cell., 98, 295, 10.1016/S0092-8674(00)81959-5 · DOI · Paper page
  4. Chen, 2005, Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function, Mol. Cell., 17, 393, 10.1016/j.molcel.2004.12.030 · DOI · Paper page
  5. Ciofani, 2012, A validated regulatory network for Th17 cell specification, Cell., 151, 289, 10.1016/j.cell.2012.09.016 · DOI · Paper page
  6. Costa-Pereira, 2002, Mutational switch of an IL-6 response to an interferon-gamma-like response, Proc. Natl. Acad. Sci. USA., 99, 8043, 10.1073/pnas.122236099 · DOI
  7. Crotty, 2014, T follicular helper cell differentiation, function, and roles in disease, Immunity., 41, 529, 10.1016/j.immuni.2014.10.004 · DOI · Paper page
  8. Delaglio, 1995, NMRPipe: a multidimensional spectral processing system based on UNIX pipes, J. Biomol. NMR., 6, 277, 10.1007/BF00197809 · DOI
  9. Ding, 2012, Three-dimensional RNA structure refinement by hydroxyl radical probing, Nat. Methods., 9, 603, 10.1038/nmeth.1976 · DOI
  10. Dong, 2014, Targeting Th17 cells in immune diseases, Cell Res., 24, 901, 10.1038/cr.2014.92 · DOI
  11. Durant, 2010, Diverse targets of the transcription factor STAT3 contribute to T cell pathogenicity and homeostasis, Immunity., 32, 605, 10.1016/j.immuni.2010.05.003 · DOI
  12. Flanagan, 2014, Activating germline mutations in STAT3 cause early-onset multi-organ autoimmune disease, Nat. Genet., 46, 812, 10.1038/ng.3040 · DOI
  13. Harris, 2007, Cutting edge: An in vivo requirement for STAT3 signaling in TH17 development and TH17-dependent autoimmunity, J. Immunol., 179, 4313, 10.4049/jimmunol.179.7.4313 · DOI
  14. Hess, 2008, GROMACS 4: Algorithms for Highly Efficient, Load-Balanced, and Scalable Molecular Simulation, J. Chem. Theory Comput., 4, 435, 10.1021/ct700301q · DOI
  15. Hong, 2002, Opposing roles of STAT1 and STAT3 in T cell-mediated hepatitis: regulation by SOCS, J. Clin. Invest., 110, 1503, 10.1172/JCI0215841 · DOI
  16. Hunter, 2015, IL-6 as a keystone cytokine in health and disease, Nat. Immunol., 16, 448, 10.1038/ni.3153 · DOI · Paper page
  17. Iwasaki, 2011, The IκB kinase complex regulates the stability of cytokine-encoding mRNA induced by TLR-IL-1R by controlling degradation of regnase-1, Nat. Immunol., 12, 1167, 10.1038/ni.2137 · DOI
  18. Kishimoto, 2005, Interleukin-6: from basic science to medicine--40 years in immunology, Annu. Rev. Immunol., 23, 1, 10.1146/annurev.immunol.23.021704.115806 · DOI
  19. Kishimoto, 2010, IL-6: from its discovery to clinical applications, Int. Immunol., 22, 347, 10.1093/intimm/dxq030 · DOI · Paper page
  20. Laurence, 2007, Interleukin-2 signaling via STAT5 constrains T helper 17 cell generation, Immunity., 26, 371, 10.1016/j.immuni.2007.02.009 · DOI · Paper page
  21. Li, 2014, Quantifying sequence and structural features of protein-RNA interactions, Nucleic Acids Res., 42, 10086, 10.1093/nar/gku681 · DOI
  22. Lin, 2014, Recent advances in the ARID family: focusing on roles in human cancer, Onco Targets Ther., 7, 315, 10.2147/OTT.S57023 · DOI
  23. Lis, 2011, Bridging the gap between single-template and fragment based protein structure modeling using Spanner, Immunome Res., 7, 1, 10.4172/1745-7580.1000041 · DOI
  24. Ma, 2014, Human T follicular helper (Tfh) cells and disease, Immunol. Cell Biol., 92, 64, 10.1038/icb.2013.55 · DOI
  25. Masuda, 2014, Th17 cells: inflammation and regulation, Atlas Genet. Cytogenet. Oncol. Haematol., 18, 611, 10.4267/2042/54019 · DOI
  26. Masuda, 2013, Arid5a controls IL-6 mRNA stability, which contributes to elevation of IL-6 level in vivo, Proc. Natl. Acad. Sci. USA., 110, 9409, 10.1073/pnas.1307419110 · DOI · Paper page
  27. Matsushita, 2009, Zc3h12a is an RNase essential for controlling immune responses by regulating mRNA decay, Nature., 458, 1185, 10.1038/nature07924 · DOI · Paper page
  28. Morita, 2000, Plat-E: an efficient and stable system for transient packaging of retroviruses, Gene Ther., 7, 1063, 10.1038/sj.gt.3301206 · DOI
  29. Muranski, 2013, Essentials of Th17 cell commitment and plasticity, Blood., 121, 2402, 10.1182/blood-2012-09-378653 · DOI
  30. Murphy, 2002, The lineage decisions of helper T cells, Nat. Rev. Immunol., 2, 933, 10.1038/nri954 · DOI
  31. Nagashima, 2014, The adaptor TRAF5 limits the differentiation of inflammatory CD4(+) T cells by antagonizing signaling via the receptor for IL-6, Nat. Immunol., 15, 449, 10.1038/ni.2863 · DOI
  32. Ng, 2013, Regulation of adaptive immunity; the role of interleukin-10, Front. Immunol., 4, 129, 10.3389/fimmu.2013.00129 · DOI
  33. O’Reilly, 2013, Interleukin-6: a new therapeutic target in systemic sclerosis?, Clin. Transl. Immunology., 2, e4, 10.1038/cti.2013.2 · DOI
  34. Saito, 2014, AT-rich-interactive domain-containing protein 5A functions as a negative regulator of retinoic acid receptor-related orphan nuclear receptor γt-induced Th17 cell differentiation, Arthritis Rheumatol., 66, 1185, 10.1002/art.38324 · DOI
  35. Salomon-Ferrer, 2013, An overview of the Amber biomolecular simulation package, Wiley Interdiscip. Rev. Comput. Mol. Sci., 3, 198, 10.1002/wcms.1121 · DOI
  36. Sharma, 2008, iFoldRNA: three-dimensional RNA structure prediction and folding, Bioinformatics., 24, 1951, 10.1093/bioinformatics/btn328 · DOI
  37. Söding, 2005, Protein homology detection by HMM-HMM comparison, Bioinformatics., 21, 951, 10.1093/bioinformatics/bti125 · DOI
  38. Stritesky, 2011, The transcription factor STAT3 is required for T helper 2 cell development, Immunity., 34, 39, 10.1016/j.immuni.2010.12.013 · DOI
  39. Tormo, 2012, IL-6 activates STAT5 in T cells, Cytokine., 60, 575, 10.1016/j.cyto.2012.07.002 · DOI
  40. Uehata, 2013, Malt1-induced cleavage of regnase-1 in CD4(+) helper T cells regulates immune activation, Cell., 153, 1036, 10.1016/j.cell.2013.04.034 · DOI · Paper page
  41. Xu, 2009, c-Maf regulates IL-10 expression during Th17 polarization, J. Immunol., 182, 6226, 10.4049/jimmunol.0900123 · DOI
  42. Yang, 2011, Opposing regulation of the locus encoding IL-17 through direct, reciprocal actions of STAT3 and STAT5, Nat. Immunol., 12, 247, 10.1038/ni.1995 · DOI · Paper page
  43. Zhou, 2007, IL-6 programs T(H)-17 cell differentiation by promoting sequential engagement of the IL-21 and IL-23 pathways, Nat. Immunol., 8, 967, 10.1038/ni1488 · DOI
  44. Zhu, 2015, An IL-27/NFIL3 signalling axis drives Tim-3 and IL-10 expression and T-cell dysfunction, Nat. Commun., 6, 6072, 10.1038/ncomms7072 · DOI
  45. Zhu, 2010, Differentiation of effector CD4 T cell populations (*), Annu. Rev. Immunol., 28, 445, 10.1146/annurev-immunol-030409-101212 · DOI · Paper page

Cited by

Sorted by citations

See all 88

Metadata

Authors
Masuda, K., Ripley, B., Nyati, K. K., Dubey, P. K., Zaman, M. M.-U., Hanieh, H., Higa, M., Yamashita, K., Standley, D. M., Mashima, T., Katahira, M., Okamoto, T., Matsuura, Y., Takeuchi, O., & Kishimoto, T.
Affiliations
  • Laboratory of Immune Regulation, World Premier International Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan 1
  • Biological Sciences Department, College of Science, King Faisal University, Al-Ahsa 31982, Saudi Arabia 3
  • Laboratory of System Immunology, World Premier International Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan 2
  • Structural Energy Bioscience Research Section, Institute of Advanced Energy, Kyoto University, Kyoto 611-0011, Japan 4
  • Department of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan 5
  • Laboratory of Infection and Prevention, Institute for Virus Research, Kyoto University, Kyoto 606-8507, Japan 6
Venue
Journal of Experimental Medicine
Published
2016-03-28
Volume
213
Issue
4
Pages
605-619
ISSN
  • 0022-1007
  • 1540-9538
Cited by
88
References
5
Language
en
Funders
  • Japan Society for the Promotion of Science (26860328)
  • Japanese Science and Technology Agency
  • Japanese Ministry of Education, Culture, Sports, Science and Technology

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