Evidence map›Paper›PMID 17360856›Full record

ArticleClinical and vaccine immunology : CVI2007

Anti-p19 antibody treatment exacerbates lyme arthritis and enhances borreliacidal activity.

Sara Heil Peterson, Dean T Nardelli, Thomas F Warner, Steven M Callister, Jose R Torrealba, Ronald F Schell

Open access · diamondAbstract read
In one paragraph

Article in Clinical and vaccine immunology : CVI, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Lyme arthritis: current concepts and a change in paradigm.Clinical and vaccine immunology : CVI · 2008
    Review
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 2 institutions in 2 countries.

Sara Heil PetersonUniversity of Wisconsin, Wisconsin State Laboratory of Hygiene, Department of Bacteriology, and Department of Pathology, Veterans Administration Hospital, Madison, WI 53706, USA.
Dean T Nardelli
Thomas F Warner
Steven M Callister
Jose R Torrealba
Ronald F Schell
Bipar · FRUniversity of Wisconsin–Madison · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Considerable effort has been made to elucidate the mechanism of Lyme arthritis. We focused on p19, a cell cycle-regulating molecule, because it is known to inhibit cell cycle division of T lymphocytes which may be responsible for the induction of arthritis. We show that anti-p19 antibody treatment enhances the inflammatory response normally detected at the tibiotarsal joints of Borrelia burgdorferi-vaccinated and Borrelia bissettii-challenged mice. Specifically, anti-p19 antibody treatment augmented the severity of inflammation within the synovial and subsynovial tissue. Moreover, treatment with anti-p19 antibody caused severe erosion of cartilage and bone with ankle joint destruction. In addition, anti-p19 antibody treatment of Borrelia-vaccinated and -challenged mice enhanced the borreliacidal antibody response, especially against the vaccine isolate. The novel activities of anti-p19 antibody show that p19 may be an important therapeutic site for the treatment of Lyme arthritis.

Indexed as

Antibodies, BacterialAntibodies, MonoclonalBorrelia burgdorferiCell Cycle ProteinsLyme DiseaseAnimalsCD4-Positive T-LymphocytesFemaleLyme Disease VaccinesMaleMiceMice, Inbred C57BLVaccinationAntibodies, BacterialAntibodies, MonoclonalCell Cycle ProteinsLyme Disease Vaccines

Identifiers

PMID17360856
PMCPMC1865634
OpenAlexW2110237954

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.