Evidence map›Paper›PMID 28724396›Full record

ArticleArthritis research & therapy2017

Pathogenic roles of CXCL10 signaling through CXCR3 and TLR4 in macrophages and T cells: relevance for arthritis.

Jong-Ho Lee, Bongjun Kim, Won Jong Jin, Hong-Hee Kim, Hyunil Ha, Zang Hee Lee

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

82 citing papers in PubMed, 139 citations in OpenAlex.

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  11. Serum cytokines in periodontal diseases.Periodontology 2000 · 2025
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  19. Modulation of CXCL10 activity as a therapeutic target of ocular toxoplasmosis in diabetic mice.Journal of parasitic diseases : official organ of the Indian Society for Parasitology · 2024
    Article
  20. Article

22 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 3 countries.

Jong-Ho LeeBrain Tumor Center and Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.
Bongjun KimDepartment of Cell and Developmental Biology, Dental Research Institute, School of Dentistry, Seoul National University, 28 Yeongon-dong, Jongno-gu, Seoul, 110-749, Republic of Korea.
Won Jong JinDepartment of Cell and Developmental Biology, Dental Research Institute, School of Dentistry, Seoul National University, 28 Yeongon-dong, Jongno-gu, Seoul, 110-749, Republic of Korea.
Hong-Hee KimDepartment of Cell and Developmental Biology, Dental Research Institute, School of Dentistry, Seoul National University, 28 Yeongon-dong, Jongno-gu, Seoul, 110-749, Republic of Korea.
Hyunil HaClinical Research Division, Korean Medicine-Based Herbal Drug Development Group, Korea Institute of Oriental Medicine, 483 Expo-Ro, Yuseong-Gu, Daejeon, 305-811, Republic of Korea. hyunil74@kiom.re.kr.
Zang Hee LeeDepartment of Cell and Developmental Biology, Dental Research Institute, School of Dentistry, Seoul National University, 28 Yeongon-dong, Jongno-gu, Seoul, 110-749, Republic of Korea. zang1959@snu.ac.kr.ORCID 0000-0003-1466-357X
Seoul National University · KRKorea Institute of Oriental Medicine · KRThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRheumatoid arthritis (RA) is a chronic autoimmune disease characterized by uncontrolled joint inflammation and destruction of bone and cartilage. We previously reported that C-X-C motif chemokine 10 (CXCL10; also called IP-10) has important roles in joint inflammation and bone destruction in arthritis. However, the specific mechanisms by which CXCL10 regulates the recruitment of inflammatory cells and the production of osteoclastogenic cytokines in RA progression are not fully understood.

methodsBone marrow-derived macrophages and CD4

resultsCXCL10 increased the migration of inflammatory cells through C-X-C chemokine receptor 3 (CXCR3)-mediated, but not toll-like receptor 4 (TLR4)-mediated, ERK activation. Interestingly, both receptors CXCR3 and TLR4 were simultaneously required for CXCL10-stimulated production of osteoclastogenic cytokines in CD4

conclusionThese findings highlight the importance of CXCL10 signaling in the pathogenesis of RA and provide previously unidentified details of the mechanisms by which CXCL10 promotes the development of arthritis.

Indexed as

AnimalsArthritis, ExperimentalArthritis, RheumatoidCD4-Positive T-LymphocytesChemokine CXCL10Chemotaxis, LeukocyteMacrophagesMiceMice, Inbred C57BLMice, KnockoutReceptors, CXCR3Signal TransductionToll-Like Receptor 4Chemokine CXCL10Cxcl10 protein, mouseCxcr3 protein, mouseReceptors, CXCR3Tlr4 protein, mouseToll-Like Receptor 4Collagen antibody-induced arthritisCXCL10CXCR3RANKLRheumatoid arthritisTLR4

Identifiers

PMID28724396
PMCPMC5518115
OpenAlexW2739115656

What OpenQuestion holds

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LicenceCC BY
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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.