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CCR2 defines in vivo development and homing of IL-23-driven GM-CSF-producing Th17 cells

Overview of attention for article published in Nature Communications, October 2015
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  • In the top 5% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (97th percentile)
  • High Attention Score compared to outputs of the same age and source (84th percentile)

Mentioned by

news
11 news outlets
blogs
2 blogs
twitter
4 X users

Citations

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107 Dimensions

Readers on

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112 Mendeley
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Title
CCR2 defines in vivo development and homing of IL-23-driven GM-CSF-producing Th17 cells
Published in
Nature Communications, October 2015
DOI 10.1038/ncomms9644
Pubmed ID
Authors

Ervin E. Kara, Duncan R. McKenzie, Cameron R. Bastow, Carly E. Gregor, Kevin A. Fenix, Abiodun D. Ogunniyi, James C. Paton, Matthias Mack, Diana R. Pombal, Cyrill Seillet, Bénédicte Dubois, Adrian Liston, Kelli P. A. MacDonald, Gabrielle T. Belz, Mark J. Smyth, Geoffrey R. Hill, Iain Comerford, Shaun R. McColl

Abstract

IL-17-producing helper T (Th17) cells are critical for host defense against extracellular pathogens but also drive numerous autoimmune diseases. Th17 cells that differ in their inflammatory potential have been described including IL-10-producing Th17 cells that are weak inducers of inflammation and highly inflammatory, IL-23-driven, GM-CSF/IFNγ-producing Th17 cells. However, their distinct developmental requirements, functions and trafficking mechanisms in vivo remain poorly understood. Here we identify a temporally regulated IL-23-dependent switch from CCR6 to CCR2 usage by developing Th17 cells that is critical for pathogenic Th17 cell-driven inflammation in experimental autoimmune encephalomyelitis (EAE). This switch defines a unique in vivo cell surface signature (CCR6(-)CCR2(+)) of GM-CSF/IFNγ-producing Th17 cells in EAE and experimental persistent extracellular bacterial infection, and in humans. Using this signature, we identify an IL-23/IL-1/IFNγ/TNFα/T-bet/Eomesodermin-driven circuit driving GM-CSF/IFNγ-producing Th17 cell formation in vivo. Thus, our data identify a unique cell surface signature, trafficking mechanism and T-cell intrinsic regulators of GM-CSF/IFNγ-producing Th17 cells.

X Demographics

X Demographics

The data shown below were collected from the profiles of 4 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 112 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Japan 1 <1%
Unknown 111 99%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 26 23%
Researcher 21 19%
Student > Master 13 12%
Student > Bachelor 10 9%
Student > Doctoral Student 7 6%
Other 18 16%
Unknown 17 15%
Readers by discipline Count As %
Immunology and Microbiology 28 25%
Agricultural and Biological Sciences 26 23%
Medicine and Dentistry 15 13%
Biochemistry, Genetics and Molecular Biology 12 11%
Neuroscience 8 7%
Other 5 4%
Unknown 18 16%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 92. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 01 September 2020.
All research outputs
#387,647
of 22,831,537 outputs
Outputs from Nature Communications
#6,625
of 47,018 outputs
Outputs of similar age
#6,367
of 284,657 outputs
Outputs of similar age from Nature Communications
#129
of 816 outputs
Altmetric has tracked 22,831,537 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 98th percentile: it's in the top 5% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 47,018 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 55.7. This one has done well, scoring higher than 85% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 284,657 tracked outputs that were published within six weeks on either side of this one in any source. This one has done particularly well, scoring higher than 97% of its contemporaries.
We're also able to compare this research output to 816 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 84% of its contemporaries.