Evidence map›Paper›PMID 25593326›Full record

ArticleJournal of leukocyte biology2015

Mycobacterium indicus pranii induces dendritic cell activation, survival, and Th1/Th17 polarization potential in a TLR-dependent manner.

Pawan Kumar, Vini John, Soumitra Marathe, Gobardhan Das, Sangeeta Bhaskar

Abstract read
In one paragraph

Article in Journal of leukocyte biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Survivin targeting triple-fusion vaccineMedical oncology (Northwood, London, England) · 2025
    Article
  2. Review
  3. Review
  4. Article
  5. Frontiers in immunology · 2024
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Cytokine Storm and Immunomodulation in COVID-19.Indian journal of critical care medicine : peer-reviewed, official publication of Indian Society of Critical Care Medicine · 2021
    Article
  11. Article
  12. Article
  13. Inflammatory Role of TLR-MyD88 Signaling in Multiple Sclerosis.Frontiers in molecular neuroscience · 2019
    Article
  14. Article
  15. Survivin: a unique target for tumor therapy.Cancer cell international · 2016
    Review
  16. Indian dermatology online journal
    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

5 authors.

Pawan Kumar*National Institute of Immunology, New Delhi, India; and International Centre for Genetic Engineering and Biotechnology, New Delhi, India.
Vini John*National Institute of Immunology, New Delhi, India; and International Centre for Genetic Engineering and Biotechnology, New Delhi, India.
Soumitra Marathe*National Institute of Immunology, New Delhi, India; and International Centre for Genetic Engineering and Biotechnology, New Delhi, India.
Gobardhan Das*National Institute of Immunology, New Delhi, India; and International Centre for Genetic Engineering and Biotechnology, New Delhi, India.
Sangeeta Bhaskar*National Institute of Immunology, New Delhi, India; and International Centre for Genetic Engineering and Biotechnology, New Delhi, India sangeeta@nii.ac.in.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MIP is a nonpathogenic, soil-borne predecessor of Mycobacterium avium. It has been reported previously that MIP possesses strong immunomodulatory properties and confers protection against experimental TB and tumor. DCs, by virtue of their unmatched antigen-presentation potential, play a critical role in activation of antitumor and antimycobacterial immune response. The effect of MIP on the behavior of DCs and the underlying mechanisms, however, have not been investigated so far. In the present study, we showed that MIP induces significant secretion of IL-6, IL-12p40, IL-10, and TNF-α by DCs and up-regulates the expression of costimulatory molecules CD40, CD80, and CD86. MIP(L) induced a significantly higher response compared with MIP(K). PI and Annexin V staining showed that MIP increases DC survival by inhibiting apoptosis. Consistently, higher expression of antiapoptotic proteins Bcl-2 and Bcl-xl was observed in MIP-stimulated DCs. Cytokines, produced by naïve T cells, cocultured with MIP-stimulated DCs, showed that MIP promotes Th1/Th17 polarization potential in DCs. Response to MIP was lost in MyD88(-/-)DCs, underscoring the critical role of TLRs in MIP-induced DC activation. Further studies revealed that TLR2 and TLR9 are involved in DC activation by MIP(L), whereas MIP(K) activates the DCs through TLR2. Our findings establish the DC activation by MIP, define the behavior of MIP-stimulated DCs, and highlight the role of TLRs in MIP-induced DC activation.

Indexed as

AnimalsBiomarkersCell PolarityCell SurvivalCytokinesDendritic CellsInflammation MediatorsMiceMycobacteriumMyeloid Differentiation Factor 88Th17 CellsTh1 CellsToll-Like Receptor 2Toll-Like Receptor 9BiomarkersCytokinesInflammation MediatorsMyeloid Differentiation Factor 88Tlr2 protein, mouseTlr9 protein, mouseToll-Like Receptor 2Toll-Like Receptor 9apoptosiscostimulatory moleculescytokinespattern recognition receptorsT cell polarization

Identifiers

PMID25593326
PMCPMC5477886

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.