Evidence map›Paper›PMID 18217945›Full record

ArticleImmunology2008

Distinct in vivo roles of CD80 and CD86 in the effector T-cell responses inducing antigen-induced arthritis.

Dragana Odobasic, Michelle T Leech, Jin R Xue, Stephen R Holdsworth

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-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

21 citing papers in PubMed, 58 citations in OpenAlex.

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  10. Samsum ant venom modulates the immune response and redox status at the acute toxic doseThe journal of venomous animals and toxins including tropical diseases · 2019
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  13. Delivery of siRNAs to Dendritic Cells Using DEC205-Targeted Lipid Nanoparticles to Inhibit Immune Responses.Molecular therapy : the journal of the American Society of Gene Therapy · 2016
    Article
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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.

Dragana OdobasicCentre for Inflammatory Diseases, Department of Medicine, Monash University, Monash Medical Centre, Clayton, Vic, Australia. dragana.odobasic@med.monash.edu.au
Michelle T Leech
Jin R Xue
Stephen R Holdsworth
Monash Medical Centre · AUMonash University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD80 and CD86 play a critical role in the initiation of T-cell responses. However, their role in the in vivo effector CD4+ T-cell responses has been less extensively investigated. The current studies have examined the functional relevance of CD80 and CD86 in the effector CD4+ T-cell responses inducing antigen-induced arthritis. Arthritis was induced in C57BL/6 mice by sensitization to methylated bovine serum albumin (mBSA) on day 0, booster immunization (day 7) and intra-articular injection of mBSA (day 21). Control or anti-CD80 and/or anti-CD86 monoclonal antibodies were administered from day 21 to day 28. Arthritis severity and immune responses were assessed on day 28. The development of arthritis was significantly suppressed by inhibition of CD80 or CD86. Blockade of both CD80 and CD86 caused a trend towards reduced disease severity compared to control antibody-treated mice. Neutralization of CD80 attenuated accumulation of CD4+ T cells in joints and enhanced splenocyte production and circulating levels of interleukin-4. Inhibition of CD86 or both CD80 and CD86 reduced T-cell accumulation in joints without affecting T helper type 1/type 2 (Th1/Th2) differentiation or antibody levels. Blockade of CD86, and not CD80, significantly suppressed splenocyte interleukin-17 (IL-17) production. These results provide further in vivo evidence that CD80 and CD86 play important pathogenic roles in effector T-cell responses. CD80 exacerbates arthritis by downregulating systemic levels of IL-4 and increasing T-cell accumulation in joints without affecting IL-17 production. CD86 enhances disease severity by upregulating IL-17 production and increasing the accumulation of effector T cells in joints without affecting Th1/Th2 development.

Indexed as

AnimalsAntibodies, MonoclonalArthritis, ExperimentalB7-1 AntigenB7-2 AntigenCD4-Positive T-LymphocytesCells, CulturedCytokinesImmunoglobulin GMacrophagesMaleMiceMice, Inbred C57BLSerum Albumin, BovineSeverity of Illness IndexSpleenAntibodies, MonoclonalB7-1 AntigenB7-2 AntigenCytokinesImmunoglobulin Gmethylated bovine serum albuminSerum Albumin, Bovine

Identifiers

PMID18217945
PMCPMC2492942
OpenAlexW1982600796

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.