Evidence map›Paper›PMID 26347474›Full record

ArticleThe Journal of experimental medicine2015

NK-DC crosstalk controls the autopathogenic Th17 response through an innate IFN-γ-IL-27 axis.

Wai Po Chong, Nicholas van Panhuys, Jun Chen, Phyllis B Silver, Yingyos Jittayasothorn, Mary J Mattapallil, Ronald N Germain, Rachel R Caspi

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

58 citing papers in PubMed, 79 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Natural Killer Cells: Dual Regulators and Therapeutic Targets in Multiple Sclerosis Immunopathogenesis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. The Immunopathogenesis of uveitis.Frontiers in medicine · 2026
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. 2-Bromo-1,4-Naphthalenedione promotes CD8Journal of neuroinflammation · 2024
    Article
  15. The role of TIM3Journal of translational internal medicine · 2024
    Article
  16. Review
  17. IL-27 attenuates IL-23 mediated inflammatory arthritis.Clinical immunology (Orlando, Fla.) · 2023
    Article
  18. Article
  19. Article
  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

8 authors at 3 institutions in 2 countries.

Wai Po ChongLaboratory of Immunology, National Eye Institute, Lymphocyte Biology Section, Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 rcaspi@helix.nih.gov waipoc@mail.nih.gov.
Nicholas van PanhuysLaboratory of Immunology, National Eye Institute, Lymphocyte Biology Section, Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.
Jun ChenState Key Laboratory of Ophthalmology, Zhongshan Ophthalmical Center, Sun Yat-sen University, Guangzhou 510060, China Laboratory of Immunology, National Eye Institute, Lymphocyte Biology Section, Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.
Phyllis B SilverLaboratory of Immunology, National Eye Institute, Lymphocyte Biology Section, Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.
Yingyos JittayasothornLaboratory of Immunology, National Eye Institute, Lymphocyte Biology Section, Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.
Mary J MattapallilLaboratory of Immunology, National Eye Institute, Lymphocyte Biology Section, Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.
Ronald N GermainLaboratory of Immunology, National Eye Institute, Lymphocyte Biology Section, Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.
Rachel R CaspiLaboratory of Immunology, National Eye Institute, Lymphocyte Biology Section, Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 rcaspi@helix.nih.gov waipoc@mail.nih.gov.
National Eye Institute · USNational Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

Genetic, Cellular and Molecular Mechanisms in Autoimmunity to RetinaZIAEY000184 · NEI · NATIONAL EYE INSTITUTE · PI CASPI, RACHEL R. · 2009 to 2025
$51.7M
Functional Biology Of T CellsZIAAI000758 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI GERMAIN, RONALD N · 2009 to 2025
$15.4M
Intramural NIH HHS
6 · The paper itself

Abstract

IFN-γ is a pathogenic cytokine involved in inflammation. Paradoxically, its deficiency exacerbates experimental autoimmune encephalomyelitis, uveitis, and arthritis. Here, we demonstrate using IFN-γ(-/-) mice repleted with IFN-γ +/+: NK cells that innate production of IFN-γ from NK cells is necessary and sufficient to trigger an endogenous regulatory circuit that limits autoimmunity. After immunization, DCs recruited IFN-γ-producing NK cells to the draining lymph node and interacted with them in a CXCR3-dependent fashion. The interaction caused DCs to produce IL-27, which in turn enhanced IFN-γ production by NK cells, forming a self-amplifying positive feedback loop. IL-10, produced by the interacting cells themselves, was able to limit this process. The NK-DC-dependent IL-27 inhibited development of the adaptive pathogenic IL-17 response and induced IL-10-producing Tr1-like cells, which ameliorated disease in an IL-10-dependent manner. Our data reveal that an early NK-DC interaction controls the adaptive Th17 response and limits tissue-specific autoimmunity through an innate IFN-γ-IL-27 axis.

Indexed as

AnimalsAutoimmune DiseasesDendritic CellsFeedback, PhysiologicalInterferon-gammaInterleukin-10InterleukinsKiller Cells, NaturalMice, Inbred C57BLMice, KnockoutReceptors, CXCR3Th17 CellsUveitisCxcr3 protein, mouseIL10 protein, mouseIl27 protein, mouseInterferon-gammaInterleukin-10InterleukinsReceptors, CXCR3

Identifiers

PMID26347474
PMCPMC4577839
OpenAlexW1912902084

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.