Evidence map›Paper›PMID 22028860›Full record

ArticlePloS one2011

IL-17RA signaling amplifies antibody-induced arthritis.

Christian D Sadik, Nancy D Kim, Elena Alekseeva, Andrew D Luster

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

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  18. CXCL5 drives neutrophil recruitment in TH17-mediated GN.Journal of the American Society of Nephrology : JASN · 2015
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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

4 authors at 2 institutions in 1 country.

Christian D SadikCenter for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy, and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.
Nancy D Kim
Elena Alekseeva
Andrew D Luster
Harvard University · USMassachusetts General Hospital · US

Funding

Sequential Control of Neutrophil Recruitment by LTB4 and Other ChemoattractantsR01AI050892 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI LUSTER, ANDREW D · 2003 to 2013
$3.9M
A non-cell autonomous requirement for neutrophil BLT1 in inflammatory arthritisK08AR054094 · NIAMS · MASSACHUSETTS GENERAL HOSPITAL · PI KIM, NANCY D · 2007 to 2011
$653k
NIAID NIH HHS R01 AI050892NIAID NIH HHS R01-AI050892NIAMS NIH HHS K08 AR054094NIAMS NIH HHS K08-AR054094
6 · The paper itself

Abstract

objectiveTo investigate the role of IL-17RA signaling in the effector phase of inflammatory arthritis using the K/BxN serum-transfer model.

methodsWild-type and Il17ra(-/-) mice were injected with serum isolated from arthritic K/BxN mice and their clinical score was recorded daily. Mice were also harvested on days 12 and 21 and ankles were analyzed for cytokine and chemokine mRNA expression by qPCR on day 12 and for bone and cartilage erosions by histology on day 21, respectively. The induction of cytokine and chemokine expression levels by IL-17A in synovial-like fibroblasts was also analyzed using qPCR.

resultsIl17ra(-/-) mice were partially protected from clinical signs of arthritis and had markedly fewer cartilage and bone erosions. The expression of several pro-inflammatory mediators, including the chemokines KC/CXCL1, MIP-2/CXCL2, LIX/CXCL5 MIP-1γ/CCL9, MCP-3/CCL7, MIP-3α/CCL20, the cytokines IL-1β, IL-6, RANKL and the matrix metalloproteinases MMP2, MMP3, and MMP13 were decreased in the ankles of Il17ra(-/-) mice compared to wild-type mice. Many of these proinflammatory genes attenuated in the ankles of Il17ra(-/-) mice were shown to be directly induced by IL-17A in synovial fibroblasts in vitro.

conclusionsIL-17RA signaling plays a role as an amplifier of the effector phase of inflammatory arthritis. This effect is likely mediated by direct activation of synovial fibroblasts by IL-17RA to produce multiple inflammatory mediators, including chemokines active on neutrophils. Therefore, interrupting IL-17RA signaling maybe a promising pharmacological target for the treatment of inflammatory arthritis.

Indexed as

Signal TransductionAnimalsAntibodiesArthritis, ExperimentalFibroblastsHumansInflammation MediatorsMatrix Metalloproteinase 3MiceNeutrophilsRANK LigandReceptors, Interleukin-17Synovial FluidAntibodiesIl17ra protein, mouseInflammation MediatorsMatrix Metalloproteinase 3RANK LigandReceptors, Interleukin-17

Identifiers

PMID22028860
PMCPMC3197623
OpenAlexW2119346564

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.