Evidence map›Paper›PMID 24172845›Full record

ArticleMucosal immunology2014

Pulmonary M. tuberculosis infection delays Th1 immunity via immunoadaptor DAP12-regulated IRAK-M and IL-10 expression in antigen-presenting cells.

M Jeyanathan, S McCormick, R Lai, S Afkhami, C R Shaler, C N Horvath, D Damjanovic, A Zganiacz, N Barra, A Ashkar and 3 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 42 citations in OpenAlex.

  1. HowVaccines · 2026
    Review
  2. Circulating antibody signatures againstFrontiers in immunology · 2026
    Article
  3. Article
  4. siRNA-MediatedInternational journal of molecular sciences · 2023
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. T Cell-Derived IL-10 Impairs Host Resistance toJournal of immunology (Baltimore, Md. : 1950) · 2017
    Article
  12. Article
  13. Article
  14. Article
  15. Antibodies and tuberculosis.Tuberculosis (Edinburgh, Scotland) · 2016
    Review
  16. Article
  17. Article
  18. Interleukin-10 Family and Tuberculosis: An Old Story Renewed.International journal of biological sciences · 2016
    Review
  19. Immunometabolism in Tuberculosis.Frontiers in immunology · 2016
    Review
  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

13 authors at 2 institutions in 1 country.

M Jeyanathan1] McMaster Immunology Research Centre and Department of Pathology and Molecular Medicine, Hamilton, Ontario, Canada [2] Michael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, Ontario, Canada.
S McCormick1] McMaster Immunology Research Centre and Department of Pathology and Molecular Medicine, Hamilton, Ontario, Canada [2] Michael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, Ontario, Canada.
R Lai1] McMaster Immunology Research Centre and Department of Pathology and Molecular Medicine, Hamilton, Ontario, Canada [2] Michael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, Ontario, Canada.
S Afkhami1] McMaster Immunology Research Centre and Department of Pathology and Molecular Medicine, Hamilton, Ontario, Canada [2] Michael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, Ontario, Canada.
C R Shaler1] McMaster Immunology Research Centre and Department of Pathology and Molecular Medicine, Hamilton, Ontario, Canada [2] Michael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, Ontario, Canada.
C N Horvath1] McMaster Immunology Research Centre and Department of Pathology and Molecular Medicine, Hamilton, Ontario, Canada [2] Michael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, Ontario, Canada.
D Damjanovic1] McMaster Immunology Research Centre and Department of Pathology and Molecular Medicine, Hamilton, Ontario, Canada [2] Michael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, Ontario, Canada.
A Zganiacz1] McMaster Immunology Research Centre and Department of Pathology and Molecular Medicine, Hamilton, Ontario, Canada [2] Michael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, Ontario, Canada.
N Barra1] McMaster Immunology Research Centre and Department of Pathology and Molecular Medicine, Hamilton, Ontario, Canada [2] Michael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, Ontario, Canada.
A Ashkar1] McMaster Immunology Research Centre and Department of Pathology and Molecular Medicine, Hamilton, Ontario, Canada [2] Michael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, Ontario, Canada.
M JordanaMcMaster Immunology Research Centre and Department of Pathology and Molecular Medicine, Hamilton, Ontario, Canada.
N AokiMcMaster Immunology Research Centre and Department of Pathology and Molecular Medicine, Hamilton, Ontario, Canada.
Z Xing1] McMaster Immunology Research Centre and Department of Pathology and Molecular Medicine, Hamilton, Ontario, Canada [2] Michael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, Ontario, Canada.
McMaster University Medical Centre · CAMcMaster University · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Interaction of mycobacteria with the host leads to retarded expression of T helper cell type 1 (Th1) immunity in the lung. However, the immune mechanisms remain poorly understood. Using in vivo and in vitro models of Mycobacterium tuberculosis (M. tb) infection, we find the immunoadaptor DAP12 (DNAX-activating protein of 12 kDa) in antigen-presenting cells (APCs) to be critically involved in this process. Upon infection of APCs, DAP12 is required for IRAK-M (interleukin-1 receptor-associated kinase M) expression, which in turn induces interleukin-10 (IL-10) and an immune-suppressed phenotype of APCs, thus leading to suppressed Th1 cell activation. Lack of DAP12 reduces APC IL-10 production and increases their Th1 cell-activating capability, resulting in expedited Th1 responses and enhanced protection. On the other hand, adoptively transferred DAP12-competent APCs suppress Th1 cell activation within DAP12-deficient hosts, and blockade of IL-10 aborts the ability of DAP12-competent APCs to suppress Th1 activation. Our study identifies the DAP12/IRAK-M/IL-10 to be a novel molecular pathway in APCs exploited by mycobacterial pathogens, allowing infection a foothold in the lung.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAntigen PresentationAntigen-Presenting CellsCytokinesDisease Models, AnimalGene Expression RegulationInflammation MediatorsInterleukin-10Interleukin-1 Receptor-Associated KinasesLungLymphocyte ActivationMaleMiceMycobacterium tuberculosisNF-kappa BAdaptor Proteins, Signal TransducingCytokinesInflammation MediatorsInterleukin-10Interleukin-1 Receptor-Associated KinasesIrak3 protein, mouseNF-kappa BTyrobp protein, mouse

Identifiers

PMID24172845
OpenAlexW2049052423

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.