Evidence map›Paper›PMID 18424728›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

Loss of STAT3 in CD4+ T cells prevents development of experimental autoimmune diseases.

Xuebin Liu, Yun Sang Lee, Cheng-Rong Yu, Charles E Egwuagu

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
157citing papers in PubMed, 2 pooled it
8.2field-weighted citation impact, top 2% 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

157 citing papers in PubMed, 2 syntheses or guidelines pooled it, 290 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. A dysbiotic microbiome triggers TScience translational medicine · 2018
    Trial
  4. Trial
  5. Janus Kinase inhibitors associated with reduced anterior uveitis risk in autoimmune diseases.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2026
    Article
  6. Article
  7. Review
  8. International journal of molecular sciences · 2026
    Article
  9. Article
  10. Article
  11. Th17 cell pathogenicity in autoimmune disease.Experimental & molecular medicine · 2025
    Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

97 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Xuebin LiuSection of Molecular Immunology, Laboratory of Immunology, National Eye Institute, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892, USA.
Yun Sang Lee
Cheng-Rong Yu
Charles E Egwuagu
National Institutes of Health · USNational Eye Institute · US

Funding

Regulation of JAK/STAT pathways in the eyeZIAEY000315 · NEI · NATIONAL EYE INSTITUTE · PI EGWUAGU, CHARLES E · 2009 to 2025
$5.4M
SOCS5 mRNA Level in PBMC: Prognostic Marker of ResponseZ01EY000315 · NEI · NATIONAL EYE INSTITUTE · PI EGWUAGU, CHARLES E · 1997 to 2008
$748k
Intramural NIH HHS Z01 EY000315
6 · The paper itself

Abstract

Th17 cells are implicated in CNS autoimmune diseases. We show that mice with targeted-deletion of Stat3 in CD4(+) T cells (CD4(Stat3)(-/-)) do not develop experimental autoimmune uveoretinitis (EAU) or experimental autoimmune encephalomyelitis. Defective Th17 differentiation noted in CD4(Stat3)(-/-) mice is compensated by exaggerated increases in Foxp3-, IL-10-, IL-4-, and IFN-gamma-expressing T cells, suggesting critical roles of STAT3 in shaping Ag-specific CD4(+) T cell repertoire. In mice with EAU, a high percentage of IL-17-expressing T cells in their peripheral lymphoid organs also secrete IFN-gamma while these double-expressors are absent in CD4(Stat3)(-/-) and wild-type mice without EAU, raising the intriguing possibility that uveitis maybe mediated by Th17 and IL-17-expressing Th1 cells. Resistance of Stat3-deficient mice to EAU derives in part from an inability of uveitogenic Th17 and Th1 cells to enter eyes or brain of the CD4(Stat3)(-/-) mouse because of the reduction in the expression of activated alpha4/beta1 integrins on CD4(Stat3)(-/-) T cells. Adoptive transfer of activated interphotoreceptor retinoid-binding protein-specific uveitogenic T cells induced in CD4(Stat3)(-/-) mice a severe EAU characterized by development of retinal folds, infiltration of inflammatory cells into the retina, and destruction of retinal architecture, underscoring our contention that the loss of STAT3 in CD4(+) T cells results in an intrinsic developmental defect that renders CD4(Stat3)(-/-) resistant to CNS inflammatory diseases. STAT3 requirement for IL-17 production by Th17, generation of double positive T cells expressing IL-17 and IFN-gamma, and for T cell trafficking into CNS tissues suggests that STAT3 may be a therapeutic target for modulating uveitis, sceritis, or multiple sclerosis.

Indexed as

Adoptive TransferAnimalsBrainCell DifferentiationCell MovementCytokinesEncephalomyelitis, Autoimmune, ExperimentalEyeForkhead Transcription FactorsIntegrin alpha4beta1MiceMice, KnockoutMultiple SclerosisSTAT3 Transcription FactorTh1 CellsUveitisCytokinesForkhead Transcription FactorsFoxp3 protein, mouseIntegrin alpha4beta1Stat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID18424728
PMCPMC2435016
OpenAlexW2119582157

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.