Evidence map›Paper›PMID 26227656›Full record

ArticleInternational journal of immunopathology and pharmacology2015

Altered Th17/Treg balance and dysregulated IL-1β response influence susceptibility/resistance to experimental autoimmune arthritis.

S H Venkatesha, S Dudics, E Weingartner, E C So, Jhf Pedra, K D Moudgil

Open access · greenAbstract read
In one paragraph

Article in International journal of immunopathology and pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Interleukin-6 (IL-6) Receptor Antagonist Protects Against Rheumatoid Arthritis.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Trial
  2. Article
  3. Review
  4. Article
  5. The role of interferon-γ in cardiovascular disease: an update.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
    Review
  6. Common innate pathways to autoimmune disease.Clinical immunology (Orlando, Fla.) · 2020
    Review
  7. Review
  8. Immunometabolism of T cells and NK cells: metabolic control of effector and regulatory function.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. 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

6 authors at 1 institution in 1 country.

S H VenkateshaDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD, USA.
S DudicsDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD, USA.
E WeingartnerDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD, USA.
E C SoDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD, USA.
Jhf PedraDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD, USA.
K D MoudgilDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD, USA Division of Rheumatology, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA kmoudgil@som.umaryland.edu.
University of Maryland, Baltimore · US

Funding

Immune Modulation of Autoimmunity by Herbal ProductsR01AT004321 · NCCIH · UNIVERSITY OF MARYLAND BALTIMORE · PI MOUDGIL, KAMAL D · 2009 to 2012
$1.5M
NCCIH NIH HHS R01 AT004321
6 · The paper itself

Abstract

This study was aimed at gaining an insight into immune mechanisms of differential susceptibility to autoimmunity of individuals sharing the same major histocompatibility complex by studying arthritis-susceptible Lewis (LEW) and arthritis-resistant Wistar Kyoto (WKY) rats (both RT.1(l)) using the adjuvant arthritis (AA) model of rheumatoid arthritis (RA). Lymph node cells (LNC) and synovium-infiltrating cells (SIC) of LEW and WKY rat subjected to an arthritogenic challenge were tested. The frequency of T helper 17 (Th17) and T regulatory (Treg) cells was determined by flow cytometry, whereas serum and spleen adherent cell (SAC)-derived supernatant were analyzed for specific cytokines and chemokines. We observed that WKY rats are not deficient in generating a Th17 response to the arthritogenic challenge in LNC (periphery); however, the Th17/Treg ratio is markedly reduced in the joint (target organ) of WKY versus LEW rats because of reduced Th17 levels therein in WKY rats. These results suggest differential and selective decrease in Th17 cell migration into the joints of WKY rats. Interestingly, serum levels of chemokines RANTES and MCP-1 were reduced in WKY rats. Furthermore, WKY rats showed reduced serum IL-1β level in vivo but no defect in IL-1β production by SAC in vitro, suggesting an effective in vivo regulation of IL-1β response. We also unraveled the role of interferon-γ (IFNγ), which we have previously reported to be increased in WKY versus LEW rats, in regulation of IL-1β. Thus, reduced Th17/Treg ratio in the target organ (joints) and decreased systemic IL-1β might contribute to the AA-resistance of WKY rats; whereas the converse factors render LEW more vulnerable to AA.

Indexed as

AnimalsArthritis, ExperimentalArthritis, RheumatoidAutoimmune DiseasesInterferon-gammaInterleukin-1betaMaleRatsRats, Inbred LewRats, Inbred WKYSpleenTh17 CellsT-Lymphocytes, RegulatoryInterferon-gammaInterleukin-1betaadjuvant arthritisarthritisautoimmunitychemokinescytokinesIFN-γIL-17IL-1βratresistancesusceptibilityTh17Treg

Identifiers

PMID26227656
PMCPMC8039840
OpenAlexW2258604382

What OpenQuestion holds

Textmetadata
LicenceTDM
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.