Evidence map›Paper›PMID 22711892›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

The T cell response to IL-10 alters cellular dynamics and paradoxically promotes central nervous system autoimmunity.

Xin Liu, Rajshekhar Alli, Meredith Steeves, Phuong Nguyen, Peter Vogel, Terrence L Geiger

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Armored human CAR TScience advances · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Autoimmunity in 2012.Clinical reviews in allergy & immunology · 2013
    Review
  17. Article
  18. 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.

Xin LiuDepartment of Pathology, St. Jude Children's Research Hospital, Memphis, TN 38120, USA.
Rajshekhar Alli
Meredith Steeves
Phuong Nguyen
Peter Vogel
Terrence L Geiger
St. Jude Children's Research Hospital · US

Funding

TREATMENT OF AUTOIMMUNITY WITH REGULATORY T LYMPHOCYTESR01AI056153 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI GEIGER, TERRENCE L · 2004 to 2013
$3.9M
NIAID NIH HHS R01 AI056153
6 · The paper itself

Abstract

IL-10 is a critical anti-inflammatory cytokine, the deficiency of which leads to spontaneous autoimmunity. However, therapeutically administered or ectopically expressed IL-10 can either suppress or promote disease. Distinct lineage-specific activities may explain the contradictory effects of IL-10. To dissect the T cell-specific response to IL-10 during organ-specific autoimmunity, we generated mice with a selective deletion of IL-10Rα in T cells and analyzed its effects in an autoimmune model, experimental allergic encephalomyelitis (EAE). Surprisingly, the T cell response to IL-10 increased EAE severity. This did not result from altered T cell functional potential; T cell cytokine profile was preserved. IL-10 also diminished the proliferation of T cells in situ within the target organ, an effect that would be expected to restrain disease. However, IL-10 acted cell autonomously to sustain the autoreactive T cells essential for immunopathogenesis, promoting their accumulation and distorting the regulatory and effector T cell balance. Indeed, in chimeric mice and after adoptive transfer, wild type T cells showed a competitive advantage over cells deficient in IL-10Rα. Therefore, T cell specific actions of IL-10 can support autoimmune inflammation, and this appears to result from an overall increase in the long term fitness of pathologic T cells. Lineage-restricted, disease-promoting activities of IL-10 should be considered in the therapeutic manipulation of the IL-10 pathway.

Indexed as

Amino Acid SequenceAnimalsCells, CulturedCoculture TechniquesEncephalomyelitis, Autoimmune, ExperimentalEpitopes, T-LymphocyteInflammation MediatorsInterleukin-10MiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMolecular Sequence DataReceptors, Interleukin-10Severity of Illness IndexSignal TransductionEpitopes, T-LymphocyteInflammation MediatorsInterleukin-10Receptors, Interleukin-10

Identifiers

PMID22711892
PMCPMC3392541
OpenAlexW2137423312

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.