Evidence map›Paper›PMID 27471636›Full record

ArticleOncoimmunology2016

CXCL16-positive dendritic cells enhance invariant natural killer T cell-dependent IFNγ production and tumor control.

Linnea Veinotte, Simon Gebremeskel, Brent Johnston

Open access · goldAbstract read
In one paragraph

Article in Oncoimmunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Article
  3. Infection and immunity · 2024
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  16. Review
  17. The Role of CXCL16 in the Pathogenesis of Cancer and Other Diseases.International journal of molecular sciences · 2021
    Review
  18. Article
  19. Review
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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

3 authors at 2 institutions in 1 country.

Linnea VeinotteDepartment of Microbiology & Immunology, Dalhousie University, Halifax, Nova Scotia, Canada; Beatrice Hunter Cancer Research Institute, Halifax, Nova Scotia, Canada.
Simon GebremeskelDepartment of Microbiology & Immunology, Dalhousie University, Halifax, Nova Scotia, Canada; Beatrice Hunter Cancer Research Institute, Halifax, Nova Scotia, Canada.
Brent JohnstonDepartment of Microbiology & Immunology, Dalhousie University, Halifax, Nova Scotia, Canada; Beatrice Hunter Cancer Research Institute, Halifax, Nova Scotia, Canada; Department of Pediatrics, Dalhousie University, Halifax, Nova Scotia, Canada; Department of Pathology, Dalhousie University, Halifax, Nova Scotia, Canada.
Beatrice Hunter Cancer Research Institute · CADalhousie University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Crosstalk interactions between dendritic cells (DCs) and invariant natural killer T (iNKT) cells are important in regulating antitumor responses elicited by glycolipid antigens. iNKT cells constitutively express the chemokine receptor CXCR6, while cytokine-activated DCs upregulate the transmembrane chemokine ligand, CXCL16. This study examined the co-stimulatory role of CXCR6/CXCL16 interactions in glycolipid-dependent iNKT cell activation and tumor control. Spleen and liver DCs in wild-type mice, but not iNKT cell deficient (Jα18(-/-)) mice, transiently upregulated surface CXCL16 following in vivo administration of the glycolipid antigen α-galactosylceramide. Recombinant CXCL16 did not directly induce iNKT cell activation in vitro but enhanced interferon (IFN)-γ production when mouse or human iNKT cells were stimulated with plate-bound anti-CD3. Compared with glycolipid-loaded CXCL16(neg) DCs, CXCL16(hi) DCs induced higher levels of IFNγ production in iNKT cell cultures and following adoptive transfer in vivo. The number of IFNγ(+) iNKT cells and expansion of T-bet(+) iNKT cells were reduced in vivo when CXCL16(-/-) DCs were used to activate iNKT cells. Enhanced IFNγ production in vivo was not dependent on CXCR6 expression on natural killer (NK) cells. Adoptive transfer of glycolipid-loaded CXCL16(hi) DCs provided superior protection against tumor metastasis compared to CXCL16(neg) DC transfers. Similarly, wild-type DCs provided superior protection against metastasis compared with CXCL16(-/-) DCs. These experiments implicate an important role for CXCR6/CXCL16 interactions in regulating iNKT cell IFNγ production and tumor control. The selective use of CXCL16(hi) DCs in adoptive transfer immunotherapies may prove useful for enhancing T helper (Th) type 1 responses and clinical outcomes in cancer patients.

Indexed as

Cell activationchemokinescytokinesdendritic cellsnatural killer T cells

Identifiers

PMID27471636
PMCPMC4938370
OpenAlexW2339252122

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.