Evidence map›Paper›PMID 26324771›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

IL-12p40 Homodimer Ameliorates Experimental Autoimmune Arthritis.

Seon-Yeong Lee, Young Ok Jung, Doo-Jin Kim, Chang-Min Kang, Young-Mee Moon, Yu-Jung Heo, Hye-Jwa Oh, Seong-Jeong Park, Se-Hwan Yang, Seung Ki Kwok and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

9 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. CD4Nature medicine · 2026
    Article
  3. Article
  4. Ebi3 Binding to IFN-γ and IL-10 Limits Their Function.Journal of immunology (Baltimore, Md. : 1950) · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
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

15 authors at 3 institutions in 1 country.

Seon-Yeong LeeRheumatism Research Center, Catholic Research Institutes of Medical Science, Catholic University of Korea, Seoul 137-701, Republic of Korea; Laboratory of Immune Network, Conversant Research Consortium in Immunologic Disease, Catholic University of Korea, Seoul 137-701, Republic of Korea;
Young Ok JungDivision of Rheumatology, Department of Internal Medicine, Hallym University Kang-Nam Sacred Heart Hospital, Seoul 150-950, Republic of Korea; and.
Doo-Jin KimIntegrative Bioscience and Biotechnology, World Class University, Pohang University of Science and Technology Biotechnology Center, Pohang University of Science and Technology, Pohang 790-784, Republic of Korea.
Chang-Min KangRheumatism Research Center, Catholic Research Institutes of Medical Science, Catholic University of Korea, Seoul 137-701, Republic of Korea;
Young-Mee MoonRheumatism Research Center, Catholic Research Institutes of Medical Science, Catholic University of Korea, Seoul 137-701, Republic of Korea; Laboratory of Immune Network, Conversant Research Consortium in Immunologic Disease, Catholic University of Korea, Seoul 137-701, Republic of Korea;
Yu-Jung HeoRheumatism Research Center, Catholic Research Institutes of Medical Science, Catholic University of Korea, Seoul 137-701, Republic of Korea;
Hye-Jwa OhRheumatism Research Center, Catholic Research Institutes of Medical Science, Catholic University of Korea, Seoul 137-701, Republic of Korea;
Seong-Jeong ParkIntegrative Bioscience and Biotechnology, World Class University, Pohang University of Science and Technology Biotechnology Center, Pohang University of Science and Technology, Pohang 790-784, Republic of Korea.
Se-Hwan YangIntegrative Bioscience and Biotechnology, World Class University, Pohang University of Science and Technology Biotechnology Center, Pohang University of Science and Technology, Pohang 790-784, Republic of Korea.
Seung Ki KwokRheumatism Research Center, Catholic Research Institutes of Medical Science, Catholic University of Korea, Seoul 137-701, Republic of Korea;
Ji-Hyeon JuRheumatism Research Center, Catholic Research Institutes of Medical Science, Catholic University of Korea, Seoul 137-701, Republic of Korea;
Sung-Hwan ParkRheumatism Research Center, Catholic Research Institutes of Medical Science, Catholic University of Korea, Seoul 137-701, Republic of Korea;
Young Chul SungIntegrative Bioscience and Biotechnology, World Class University, Pohang University of Science and Technology Biotechnology Center, Pohang University of Science and Technology, Pohang 790-784, Republic of Korea.
Ho-Youn KimRheumatism Research Center, Catholic Research Institutes of Medical Science, Catholic University of Korea, Seoul 137-701, Republic of Korea; iammila@catholic.ac.kr ho0919@catholic.ac.kr.
Mi-La ChoRheumatism Research Center, Catholic Research Institutes of Medical Science, Catholic University of Korea, Seoul 137-701, Republic of Korea; Laboratory of Immune Network, Conversant Research Consortium in Immunologic Disease, Catholic University of Korea, Seoul 137-701, Republic of Korea; iammila@catholic.ac.kr ho0919@catholic.ac.kr.
Catholic University of Korea · KRPohang University of Science and Technology · KRHallym University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IL-23 is the key cytokine that induces the expansion of Th17 cells. It is composed of p19 and p40 subunits of IL-12. The p40 subunit binds competitively to the receptor of IL-23 and blocks its activity. Our aim was to assess the preventive and therapeutic effect of the IL-12p40 homodimer (p40)2 subunit in autoimmune arthritis animal models. In the current study, using IL-1R antagonist-knockout mice and a collagen-induced arthritis model, we investigated the suppressive effect of (p40)2 on inflammatory arthritis. We demonstrated that the recombinant adenovirus-expressing mouse (p40)2 model prevented the development of arthritis when given before the onset of arthritis. It also decreased the arthritis index and joint erosions in the mouse model if transferred after arthritis was established. (p40)2 inhibited the production of inflammatory cytokines and Ag-specific T cell proliferation. It also induced CD4(+)CD25(+)Foxp3 regulatory T (Treg) cells in vitro and in vivo, whereas the generation of retinoic acid receptor-related organ receptor γt and Th17 cells was suppressed. The induction of Treg cells and the suppression of Th17 cells were mediated via activated STAT5 and suppressed STAT3. Our data suggest that (p40)2 suppressed inflammatory arthritis successfully. This could be a useful therapeutic approach in autoimmune arthritis to regulate the Th17/Treg balance and IL-23 signaling.

Indexed as

AnimalsArthritis, ExperimentalCell ProliferationCells, CulturedCollagenCytokinesInterleukin-12 Subunit p40Interleukin-17Interleukin-23 Subunit p19Lymphocyte ActivationMaleMiceMice, Inbred DBAMice, KnockoutNuclear Receptor Subfamily 1, Group F, Member 1Protein MultimerizationCollagenCytokinesIl17a protein, mouseIL1R1 protein, mouseIl23a protein, mouseInterleukin-12 Subunit p40Interleukin-17Interleukin-23 Subunit p19Nuclear Receptor Subfamily 1, Group F, Member 1Receptors, InterleukinReceptors, Interleukin-1 Type IRora protein, mouseStat3 protein, mouseSTAT3 Transcription FactorStat5a protein, mouseSTAT5 Transcription Factor

Identifiers

PMID26324771
PMCPMC4574520
OpenAlexW1916449534

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.