Evidence map›Paper›PMID 27160252›Full record

ArticleClinical and experimental medicine2017

APL-1, an altered peptide ligand derived from heat-shock protein, alone or combined with methotrexate attenuates murine collagen-induced arthritis.

Norailys Lorenzo, Fiorella Altruda, Lorenzo Silengo, Maria Del Carmen Dominguez

Abstract read
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In one paragraph

Article in Clinical and experimental medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Trial
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  3. Molecular Chaperonin HSP60: Current Understanding and Future Prospects.International journal of molecular sciences · 2024
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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 1 institution in 1 country.

Norailys LorenzoBiomedical Research Department, Center for Genetic Engineering and Biotechnology, P.O. Box 6162, 10600, Havana, Cuba.
Fiorella AltrudaDepartment of Genetics, Biology and Biochemistry, Molecular Biotechnology Center, Turin, Italy.
Lorenzo SilengoDepartment of Genetics, Biology and Biochemistry, Molecular Biotechnology Center, Turin, Italy.
Maria Del Carmen DominguezBiomedical Research Department, Center for Genetic Engineering and Biotechnology, P.O. Box 6162, 10600, Havana, Cuba. mcarmen.dominguez@cigb.edu.cu.
Centro de Ingeniería Genética y Biotecnología · CU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Induction of tolerance to autoantigens in vivo is a complex process that involves several mechanisms such as the induction of regulatory T cells and changes in the cytokine and chemokine profiles. This approach represents an attractive alternative for treatment of autoimmune diseases. APL-1 is an altered peptide ligand derived from a novel CD4 + T cell epitope of human heat-shock protein of 60 kDa (HSP60), an autoantigen involved in the pathogenesis of rheumatoid arthritis (RA). We have shown previously that this peptide efficiently inhibited the course of adjuvant-induced arthritis in Lewis rats and induced regulatory T cell (Treg) in ex vivo assay with PBMC isolated from RA patients. This study was undertaken to evaluate the therapeutic effect of APL-1 and its combination with methotrexate (MTX) in collagen-induced arthritis (CIA). CIA was induced in male DBA/1 mice at 8 weeks of age by immunization with chicken collagen. APL, MTX or both were administrated beginning from arthritis onset. Therapeutic effect was evaluated by arthritis and joint pathologic scores. In addition, TNFα and IL-10 in sera were measured by ELISA. Treg induction was assessed by FACS analysis. APL-1 inhibits efficiently the course of arthritis in CIA, similar to MTX. In addition, therapy with APL-1 plus MTX reduced CIA in mice, associated with an increase in Treg. These facts reinforce the therapeutic possibilities of APL-1 as a candidate drug for treatment of RA.

Indexed as

AnimalsArthritis, ExperimentalDisease Models, AnimalDrug Therapy, CombinationEnzyme-Linked Immunosorbent AssayFlow CytometryHeat-Shock ProteinsImmunologic FactorsInterleukin-10MaleMethotrexateMice, Inbred DBAPeptidesSeverity of Illness IndexT-Lymphocytes, RegulatoryTreatment OutcomeHeat-Shock ProteinsImmunologic FactorsInterleukin-10MethotrexatePeptidesTumor Necrosis Factor-alphaAPLCollagen-induced arthritisHSP60Rheumatoid arthritisTreg

Identifiers

PMID27160252
OpenAlexW2346657941

What OpenQuestion holds

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Read underepoch 390

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.