Evidence map›Paper›PMID 18462718›Full record

ReviewExperimental and molecular pathology2008

Gene expression profiling provides insights into the pathways involved in inflammatory arthritis development: murine model of Lyme disease.

Jennifer C Miller, Ying Ma, Hillary Crandall, Xiaohui Wang, Janis J Weis

Open access · greenAbstract readReview
In one paragraph

Review in Experimental and molecular pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

26 citing papers in PubMed, 32 citations in OpenAlex.

  1. Trial
  2. Strain-specific immune response patterns toInfection and immunity · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Immune Response toCurrent issues in molecular biology · 2021
    Article
  11. Protection againstHuman vaccines & immunotherapeutics · 2020
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Phagosomal TLR signaling upon Borrelia burgdorferi infection.Frontiers in cellular and infection microbiology · 2014
    Review
  20. 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

5 authors at 1 institution in 1 country.

Jennifer C MillerDepartment of Pathology, University of Utah, Salt Lake City, Utah 84112, USA.
Ying Ma
Hillary Crandall
Xiaohui Wang
Janis J Weis
University of Utah · US

Funding

UTAH REGIONAL CANCER CENTERP30CA042014 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Jared P Rutter · 1986 to 2026
$72.6M
MOLECULAR GENETICS OF LYME ARTHRITIS SUSCEPTIBILITYR01AR043521 · NIAMS · UNIVERSITY OF UTAH · PI WEIS, JANIS J. · 1994 to 2024
$9.4M
RESEARCH TRAINING IN HEMATOLOGYT32DK007115 · NIDDK · UNIVERSITY OF UTAH · PI LEIBOLD, ELIZABETH ANN, PRCHAL, JOSEF T · 1986 to 2020
$8.4M
BORRELIA BURGDORFERI MITOGEN IN DEVELOPMENT OF ARTHRITISR01AI032223 · NIAID · UNIVERSITY OF UTAH · PI WEIS, JANIS J. · 1993 to 2023
$7.8M
Training Program in Microbial PathogenesisT32AI055434 · NIAID · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI MULVEY, MATTHEW A, PLANELLES, VICENTE · 2004 to 2025
$6.0M
Borrelia Burgdorferi Mitogen in Development of ArthritisR56AI032223 · NIAID · UNIVERSITY OF UTAH · PI WEIS, JANIS J. · 2013 to 2013
$350k
NCI NIH HHS 5P30CA42014NCI NIH HHS P30 CA042014NIAID NIH HHS 5T32-AI055434NIAID NIH HHS AI-32223NIAID NIH HHS R01 AI032223NIAID NIH HHS R56 AI032223NIAID NIH HHS T32 AI055434NIAMS NIH HHS AR-43521NIAMS NIH HHS R01 AR043521NIDDK NIH HHS DK07115NIDDK NIH HHS T32 DK007115
6 · The paper itself

Abstract

The spirochete Borrelia burgdorferi, the etiologic agent of Lyme disease, causes severe subacute arthritis in susceptible inbred mouse strains, such as C3H/HeN, but only mild arthritis in resistant strains such as C57BL/6. The degree of Lyme arthritis severity is controlled in part by host genetics and several quantitative trait loci have been identified which contribute to this regulation. In addition, the anti-inflammatory cytokine IL-10 assumes an important role in the control of arthritis in C57BL/6 mice. However, the identification of genes and signaling pathways that dictate arthritis severity has remained elusive. In an attempt to elucidate such genes and pathways, the power of microarray analysis was combined with information gleaned from gene manipulation models. As a result of this approach, two novel gene profiles were identified: an IFN-inducible profile in arthritis-susceptible C3H and IL-10(-/-) mice, and an epidermal/differentiation profile in C57BL/6 mice. Application of this information to TLR2(-/-) mice, which also develop severe arthritis, indicated that they also upregulated IFN-responsive genes. These results provided new insight into the regulation of Lyme arthritis development and illustrated the utility of combining gene expression analyses with genetically manipulated mouse models in unraveling mechanisms underlying specific disease processes.

Indexed as

Disease Models, AnimalMiceAnimalsArthritisBorrelia burgdorferiGene Expression ProfilingInterferonsLyme DiseaseNF-kappa BInterferonsNF-kappa B

Identifiers

PMID18462718
PMCPMC2565650
OpenAlexW2077402695

What OpenQuestion holds

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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.