Evidence map›Paper›PMID 28518215›Full record

ArticleImmunology2017

The Toll-like receptor 9 signalling pathway regulates MR1-mediated bacterial antigen presentation in B cells.

Jianyun Liu, Randy R Brutkiewicz

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. The MR1/MAIT cell axis in CNS diseases.Brain, behavior, and immunity · 2024
    Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Overcoming Barriers for siRNA Therapeutics: From Bench to Bedside.Pharmaceuticals (Basel, Switzerland) · 2020
    Review
  14. MAIT Cell Activation and Functions.Frontiers in immunology · 2020
    Review
  15. Mucosal-Associated Invariant T cell in liver diseases.International journal of biological sciences · 2020
    Review
  16. Article
  17. Article
  18. MAIT cells and viruses.Immunology and cell biology · 2018
    Review
  19. Review
  20. Review
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

2 authors at 2 institutions in 1 country.

Jianyun LiuDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, USA.
Randy R BrutkiewiczDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, USA.
Indiana University – Purdue University Indianapolis · USIndiana University School of Medicine

Funding

Tumor Microenvironment and Metastasis ProgramP30CA082709 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI Jun Wan · 1999 to 2026
$59.3M
Project-005U54DK106846 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI Reuben Kapur, Karen Elizabeth Pollok · 2015 to 2026
$9.7M
Immune Evasion by Multiple Myeloma: Role of the Rho Kinase Signaling PathwayR01CA161178 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI BRUTKIEWICZ, RANDY R · 2012 to 2016
$1.6M
NCI NIH HHS P30 CA082709NCI NIH HHS R01 CA161178NIDDK NIH HHS U54 DK106846
6 · The paper itself

Abstract

Mucosal-associated invariant T (MAIT) cells are conserved T cells that express a semi-invariant T-cell receptor (Vα7.2 in humans and Vα19 in mice). The development of MAIT cells requires the antigen-presenting MHC-related protein 1 (MR1), as well as commensal bacteria. The mechanisms that regulate the functional expression of MR1 molecules and their loading with bacterial antigen in antigen-presenting cells are largely unknown. We have found that treating B cells with the Toll-like receptor 9 (TLR9) agonist CpG increases MR1 surface expression. Interestingly, activation of TLR9 by CpG-A (but not CpG-B) enhances MR1 surface expression. This is limited to B cells and not other types of cells such as monocytes, T or natural killer cells. Knocking-down TLR9 expression by short hairpin RNA reduces MR1 surface expression and MR1-mediated bacterial antigen presentation. CpG-A triggers early endosomal TLR9 activation, whereas CpG-B is responsible for late endosomal/lysosomal activation of TLR9. Consistently, blocking endoplasmic reticulum to Golgi protein transport, rather than lysosomal acidification, suppressed MR1 antigen presentation. Overall, our results indicate that early endosomal TLR9 activation is important for MR1-mediated bacterial antigen presentation.

Indexed as

Antigen PresentationLymphocyte ActivationAntigens, BacterialB-LymphocytesCell Line, TumorCpG IslandsEndoplasmic ReticulumEndosomesGolgi ApparatusHistocompatibility Antigens Class IHumansHydrogen-Ion ConcentrationLysosomesMinor Histocompatibility AntigensOligonucleotidesProtein TransportAntigens, BacterialHistocompatibility Antigens Class IMinor Histocompatibility AntigensMR1 protein, humanOligonucleotidesTLR9 protein, humanToll-Like Receptor 9antigen presentation/processingbacterialB cellssignal transductionToll-like receptors

Identifiers

PMID28518215
PMCPMC5588774
OpenAlexW2614753096

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.