Evidence map›Paper›PMID 28768901›Full record

ArticleJCI insight2017

Essential role for CCR6 in certain inflammatory diseases demonstrated using specific antagonist and knockin mice.

Remy Robert, Caroline Ang, Guizhi Sun, Laurent Juglair, Ee X Lim, Linda J Mason, Natalie L Payne, Claude Ca Bernard, Charles R Mackay

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
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  15. Interleukin-17A and Keratinocytes in Psoriasis.International journal of molecular sciences · 2020
    Review
  16. Article
  17. Review
  18. Is CCR6 Required for the Development of Psoriasiform Dermatitis in Mice?The Journal of investigative dermatology · 2019
    Article
  19. CNS infection and immune privilege.Nature reviews. Neuroscience · 2018
    Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Remy RobertDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Australia.
Caroline AngDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Australia.
Guizhi SunAustralian Regenerative Medicine Institute, Monash University, Victoria, Australia.
Laurent JuglairDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Australia.
Ee X LimDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Australia.
Linda J MasonDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Australia.
Natalie L PayneAustralian Regenerative Medicine Institute, Monash University, Victoria, Australia.
Claude Ca BernardAustralian Regenerative Medicine Institute, Monash University, Victoria, Australia.
Charles R MackayDepartment of Microbiology, Biomedicine Discovery Institute, Monash University, Clayton, Australia.
Monash University · AUAustralian Regenerative Medicine Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The chemokine receptor CCR6 marks subsets of T cells and innate lymphoid cells that produce IL-17 and IL-22, and as such may play a role in the recruitment of these cells to certain inflammatory sites. However, the precise role of CCR6 has been controversial, in part because no effective monoclonal antibody (mAb) inhibitors against this receptor exist for use in mouse models of inflammation. We circumvented this problem using transgenic mice expressing human CCR6 (hCCR6) under control of its native promoter (hCCR6-Tg/mCCR6-/-). We also developed a fully humanized mAb against hCCR6 with antagonistic activity. The expression pattern of hCCR6 in hCCR6-Tg/mCCR6-/- mice was consistent with the pattern observed in humans. In mouse models of experimental autoimmune encephalomyelitis (EAE) and psoriasis, treatment with anti-hCCR6 mAb was remarkably effective in both preventive and therapeutic regimens. For instance, in the imiquimod model of psoriasis, anti-CCR6 completely abolished all signs of inflammation. Moreover, anti-hCCR6 attenuated clinical symptoms of myelin oligodendrocyte glycoprotein-induced (MOG-induced) EAE and reduced infiltration of inflammatory cells in the central nervous system. CCR6 plays a critical role in Th17 type inflammatory reactions, and CCR6 inhibition may offer an alternative approach for the treatment of these lesions.

Indexed as

AutoimmunityTherapeutics

Identifiers

PMID28768901
PMCPMC5543919
OpenAlexW2739600521

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.