Evidence map›Paper›PMID 18606638›Full record

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

Impaired SLAM-SLAM homotypic interaction between invariant NKT cells and dendritic cells affects differentiation of IL-4/IL-10-secreting NKT2 cells in nonobese diabetic mice.

Denis V Baev, Simone Caielli, Francesca Ronchi, Margherita Coccia, Federica Facciotti, Kim E Nichols, Marika Falcone

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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 16% 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, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. The transcriptional programs of iNKT cells.Seminars in immunology · 2015
    Review
  11. iNKT and MAIT Cell Alterations in Diabetes.Frontiers in immunology · 2015
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  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

7 authors at 2 institutions in 2 countries.

Denis V BaevExperimental Diabetes Unit, San Raffaele Scientific Institute, Milan, Italy.
Simone Caielli
Francesca Ronchi
Margherita Coccia
Federica Facciotti
Kim E Nichols
Marika Falcone
Vita-Salute San Raffaele University · ITChildren's Hospital of Philadelphia · US

Funding

NKT cell-mediated modulation of autoimmune diabetesR01DK065128 · NIDDK · FONDAZONE CENT/SAN RAFFAELE/DEL MONTE · PI FALCONE, MARIKA MC · 2006 to 2008
$316k
NIDDK NIH HHS R01 DK065128NIDDK NIH HHS R01 DK65128Telethon GJT04011
6 · The paper itself

Abstract

The regulatory function of invariant NKT (iNKT) cells for tolerance induction and prevention of autoimmunity is linked to a specific cytokine profile that comprises the secretion of type 2 cytokines like IL-4 and IL-10 (NKT2 cytokine profile). The mechanism responsible for iNKT cell differentiation toward a type 2 phenotype is unknown. Herein we show that costimulatory signals provided by the surface receptor signaling lymphocytic activation molecule (SLAM) on myeloid dendritic cells (mDC) to iNKT cells is crucial for NKT2 orientation. Additionally, we demonstrate that the impaired acquisition of an NKT2 cytokine phenotype in nonobese diabetic (NOD) mice that spontaneously develop autoimmune diabetes is due to defective SLAM-induced signals generated by NOD mDC. Mature mDC of C57BL/6 mice express SLAM and induce C57BL/6 or NOD iNKT cells to acquire a predominant NKT2 cytokine phenotype in response to antigenic stimulation with the iNKT cell-specific Ag, the alpha-galactosylceramide. In contrast, mature NOD mDC express significantly lower levels of SLAM and are unable to promote GATA-3 (the SLAM-induced intracellular signal) up-regulation and IL-4/IL-10 production in iNKT cells from NOD or C57BL/6 mice. NOD mice carry a genetic defect of the Slamf1 gene that is associated with reduced SLAM expression on double-positive thymocytes and altered iNKT cell development in the thymus. Our data suggest that the genetic Slamf1 defect in NOD mice also affects SLAM expression on other immune cells such as the mDC, thus critically impairing the peripheral differentiation of iNKT cells toward a regulatory NKT2 type.

Indexed as

AnimalsAntigens, CDCell DifferentiationDendritic CellsGATA3 Transcription FactorInterleukin-10Interleukin-4Killer Cells, NaturalMiceMice, Inbred C57BLMice, Inbred NODReceptors, Cell SurfaceSignaling Lymphocytic Activation Molecule Family Member 1T-Lymphocyte SubsetsAntigens, CDGata3 protein, mouseGATA3 Transcription FactorInterleukin-10Interleukin-4Receptors, Cell SurfaceSignaling Lymphocytic Activation Molecule Family Member 1Slamf1 protein, mouse

Identifiers

PMID18606638
PMCPMC2587206
OpenAlexW2076671118

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.