Evidence map›Paper›PMID 25420916›Full record

Trial reportJournal of leukocyte biology2015

Induction of indoleamine 2,3-dioxygenase by Borrelia burgdorferi in human immune cells correlates with pathogenic potential.

Andrea C Love, Ira Schwartz, Mary M Petzke

Open access · greenAbstract readClinical Trial
In one paragraph

Trial report in Journal of leukocyte biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 37% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Insights From Omics in Lyme Disease.The Journal of infectious diseases · 2024
    Review
  3. Article
  4. Immune Response toCurrent issues in molecular biology · 2021
    Article
  5. Article
  6. TLR7 activation in epilepsy of tuberous sclerosis complex.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Article
  7. Article
  8. Article
  9. Article
  10. Suicide and Lyme and associated diseases.Neuropsychiatric disease and treatment · 2017
    Article
  11. Article
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

3 authors at 1 institution in 1 country.

Andrea C LoveDepartment of Microbiology and Immunology, New York Medical College, Valhalla, New York, USA.
Ira SchwartzDepartment of Microbiology and Immunology, New York Medical College, Valhalla, New York, USA.
Mary M PetzkeDepartment of Microbiology and Immunology, New York Medical College, Valhalla, New York, USA mary_petzke@nymc.edu.
New York Medical College · US

Funding

NCEZID CDC HHS 5U01CK000153NCEZID CDC HHS U01 CK000153
6 · The paper itself

Abstract

Borrelia burgdorferi, the bacterial agent of Lyme disease, induces the production of type I IFNs by human DCs through TLR7 and TLR9 signaling. This type I IFN response occurs in a genotype-dependent manner, with significantly higher levels of IFN-α elicited by B. burgdorferi strains that have a greater capacity for causing disseminated infection. A B. burgdorferi strain that was previously shown to induce IFN-α was found to elicit significantly higher levels of IDO1 protein and its downstream metabolite, kynurenine, compared with a B. burgdorferi mutant that lacks a single linear plasmid (lp36); this mutant is unable to induce IFN-α and is severely attenuated for infectivity in mice. Production of IDO by mDC and pDC populations, present within human PBMCs, was concomitant with increased expression of the DC maturation markers, CD83 and CCR7. The defects in IDO production and expression of CD83 and CCR7 could be restored by complementation of the mutant with lp36. Maximal IDO production in response to the wild-type strain was dependent on contributions by both type I IFN and IFN-γ, the type II IFN. Induction of IDO was mediated by the same TLR7-dependent recognition of B. burgdorferi RNA that contributes to the production of type I IFNs by human DCs. The ability of IFN-α-inducing B. burgdorferi strains to stimulate production of IDO and kynurenines may be a mechanism that is used by the pathogen to promote localized immunosuppression and facilitate hematogenous dissemination.

Indexed as

AdultAgedAnimalsAntigens, CDBorrelia burgdorferiCD83 AntigenDendritic CellsEnzyme InductionFemaleHumansImmunoglobulinsIndoleamine-Pyrrole 2,3,-DioxygenaseInterferon-alphaInterferon-gammaLeukocytes, MononuclearLyme DiseaseAntigens, CDCCR7 protein, humanCD83 AntigenIDO1 protein, humanIFNG protein, humanImmunoglobulinsIndoleamine-Pyrrole 2,3,-DioxygenaseInterferon-alphaInterferon-gammaMembrane GlycoproteinsReceptors, CCR7TLR7 protein, humanToll-Like Receptor 7bacteriumdendritic cellsimmunosuppressionLyme disease

Identifiers

PMID25420916
PMCPMC4304421
OpenAlexW2070564917

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.