Evidence map›Paper›PMID 32307907›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2020

Attenuation of Murine Collagen-Induced Arthritis by Targeting CD6.

Yan Li, Jeffrey H Ruth, Stephanie M Rasmussen, Kalana S Athukorala, Daniel P Weber, M Asif Amin, Phillip L Campbell, Nora G Singer, David A Fox, Feng Lin

Open access · bronzeAbstract read
In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 27 citations in OpenAlex.

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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

10 authors at 3 institutions in 1 country.

Yan LiCleveland Clinic, Cleveland, Ohio.
Jeffrey H RuthUniversity of Michigan, Ann Arbor.ORCID 0000-0002-9646-0321
Stephanie M RasmussenUniversity of Michigan, Ann Arbor.
Kalana S AthukoralaUniversity of Michigan, Ann Arbor.
Daniel P WeberUniversity of Michigan, Ann Arbor.
M Asif AminUniversity of Michigan, Ann Arbor.
Phillip L CampbellUniversity of Michigan, Ann Arbor.
Nora G SingerMetroHealth Medical Center, Cleveland, Ohio.
David A FoxUniversity of Michigan, Ann Arbor.
Feng LinCleveland Clinic, Cleveland, Ohio.
University of Michigan · USCleveland Clinic · USMetroHealth · US

Funding

Role of CD6 in the pathogenesis of autoimmune uveitisR01EY025373 · NEI · CLEVELAND CLINIC LERNER COM-CWRU · PI LIN, FENG C · 2017 to 2021
$2.0M
Development of a novel antibody-drug conjugate for treating T-cell lymphoma.R41CA275639 · NCI · ABCON THERAPEUTICS, INC. · PI LIN, FENG C · 2022 to 2022
$403k
NCI NIH HHS R41 CA275639NEI NIH HHS R01 EY025373
6 · The paper itself

Abstract

objectiveCD6 is an important regulator of T cell function that interacts with the ligands CD166 and CD318. To further clarify the significance of CD6 in rheumatoid arthritis (RA), we examined the effects of targeting CD6 in the mouse model of collagen-induced arthritis (CIA), using CD6-knockout (CD6-KO) mice and CD6-humanized mice that express human CD6 in lieu of mouse CD6 on their T cells.

methodsWe immunized wild-type (WT) and CD6 gene-KO mice with a collagen emulsion to induce CIA. For treatment studies using CD6-humanized mice, mice were immunized similarly and a mouse anti-human CD6 IgG (UMCD6) or control IgG was injected on days 7, 14, and 21. Joint tissues were evaluated for tissue damage, leukocyte infiltration, and local inflammatory cytokine production. Collagen-specific Th1, Th9, and Th17 responses and serum levels of collagen-specific IgG subclasses were also evaluated in WT and CD6-KO mice with CIA.

resultsThe absence of CD6 reduced 1) collagen-specific Th9 and Th17, but not Th1 responses, 2) the levels of many proinflammatory joint cytokines, and 3) serum levels of collagen-reactive total IgG and IgG1, but not IgG2a and IgG3. Joint homogenate hemoglobin content was significantly reduced in CD6-KO mice with CIA compared to WT mice with CIA (P < 0.05) (reduced angiogenesis). Moreover, treating CD6-humanized mice with mouse anti-human CD6 monoclonal antibody was similarly effective in reducing joint inflammation in CIA.

conclusionTaken together, these data suggest that interaction of CD6 with its ligands is important for the perpetuation of CIA and other inflammatory arthritides that are T cell driven.

Indexed as

AnimalsAnkle JointAntigens, CDAntigens, Differentiation, T-LymphocyteArthritis, ExperimentalCollagen Type IICytokinesHemoglobinsImmunoglobulin GMiceMice, Inbred DBAMice, KnockoutMice, TransgenicNeovascularization, PathologicTh17 CellsTh1 CellsAntigens, CDAntigens, Differentiation, T-LymphocyteCD6 antigenCollagen Type IICytokinesHemoglobinsImmunoglobulin G

Identifiers

PMID32307907
PMCPMC7745675
OpenAlexW3016518173

What OpenQuestion holds

Textmetadata
LicenceTDM
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.