Evidence map›Paper›PMID 22578563›Full record

ArticleJournal of autoimmunity2012

Definition of IFN-γ-related pathways critical for chemically-induced systemic autoimmunity.

K Michael Pollard, Per Hultman, Christopher B Toomey, David M Cauvi, Hal M Hoffman, John C Hamel, Dwight H Kono

Open access · greenAbstract read
In one paragraph

Article in Journal of autoimmunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Effect of Age on Xenobiotic-Induced Autoimmunity.bioRxiv : the preprint server for biology · 2025
    Article
  3. Article
  4. Mercury-induced inflammation and autoimmunity.Biochimica et biophysica acta. General subjects · 2019
    Review
  5. Article
  6. Environmental Xenobiotic Exposure and Autoimmunity.Current opinion in toxicology · 2018
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Silica, Silicosis, and Autoimmunity.Frontiers in immunology · 2016
    Review
  13. Article
  14. Article
  15. Cathepsin B regulates the appearance and severity of mercury-induced inflammation and autoimmunity.Toxicological sciences : an official journal of the Society of Toxicology · 2014
    Article
  16. Article
  17. Review
  18. Autoimmunity in 2012.Clinical reviews in allergy & immunology · 2013
    Review
  19. Review
  20. 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

7 authors at 3 institutions in 2 countries.

K Michael PollardDepartment of Molecular and Experimental Medicine, MEM125, Scripps Research Institute, La Jolla, CA 92037, USA. mpollard@scripps.edu
Per Hultman
Christopher B Toomey
David M Cauvi
Hal M Hoffman
John C Hamel
Dwight H Kono
Scripps Research Institute · USLinköping University · SEUniversity of California, San Diego · US

Funding

The Role of Cryopyrin in Autoinflammatory DiseasesR01AI052430 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HOFFMAN, HAROLD M · 2002 to 2011
$3.4M
Defining the effector gene repertoire in systemic autoimmunity by ENU mutagenesisR01AR053731 · NIAMS · SCRIPPS RESEARCH INSTITUTE, THE · PI KONO, DWIGHT H · 2007 to 2011
$2.5M
MERCURY INDUCED AUTOIMMUNITYR01ES007511 · NIEHS · SCRIPPS RESEARCH INSTITUTE, THE · PI POLLARD, KENNETH MICHAEL · 1997 to 2007
$2.1M
Role of Daf in Systemic AutoimmunityR01ES014847 · NIEHS · SCRIPPS RESEARCH INSTITUTE, THE · PI POLLARD, KENNETH MICHAEL · 2008 to 2012
$1.9M
NIAID NIH HHS AI052430NIAID NIH HHS R01 AI052430NIAMS NIH HHS AR053731NIAMS NIH HHS R01 AR053731NIEHS NIH HHS ES007511NIEHS NIH HHS ES014847NIEHS NIH HHS R01 ES007511NIEHS NIH HHS R01 ES014847
6 · The paper itself

Abstract

IFN-γ is essential for idiopathic and murine mercury-induced systemic autoimmunity (mHgIA), and heterozygous IFN-γ(+/-) mice also exhibit reduced disease. This suggests that blocking specific IFN-γ-related pathways that may only partially inhibit IFN-γ production or function will also suppress autoimmunity. To test this hypothesis, mice deficient in genes regulating IFN-γ expression (Casp1, Nlrp3, Il12a, Il12b, Stat4) or function (Ifngr1, Irf1) were examined for mHgIA susceptibility. Absence of either Ifngr1 or Irf1 resulted in a striking reduction of disease, while deficiency of genes promoting IFN-γ expression had modest to no effect. Furthermore, both Irf1- and Ifng-deficiency only modestly reduced the expansion of CD44(hi) and CD44(hi)CD55(lo) CD4(+) T cells, indicating that they are not absolutely required for T cell activation. Thus, there is substantial redundancy in genes that regulate IFN-γ expression in contrast to those that mediate later signaling events. These findings have implications for the therapeutic targeting of IFN-γ pathways in systemic autoimmunity.

Indexed as

AnimalsAntigens, CDAutoimmune DiseasesAutoimmunityCell ProliferationGene DeletionGene Expression RegulationHeterozygoteInjections, SubcutaneousInterferon-gammaMercuric ChlorideMiceMice, Inbred C57BLMice, TransgenicSignal TransductionT-LymphocytesAntigens, CDInterferon-gammaMercuric Chloride

Identifiers

PMID22578563
PMCPMC3570757
OpenAlexW2083040532

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.