Evidence map›Paper›PMID 24695099›Full record

ArticlePloS one2014

Immune subversion by Mycobacterium tuberculosis through CCR5 mediated signaling: involvement of IL-10.

Shibali Das, Sayantan Banerjee, Saikat Majumder, Bidisha Paul Chowdhury, Avranil Goswami, Kuntal Halder, Urmita Chakraborty, Nishith K Pal, Subrata Majumdar

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. 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
2.3field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 40 citations in OpenAlex.

  1. Epigenetic Reprogramming byAntibiotics (Basel, Switzerland) · 2026
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  3. Negative Regulation of Autophagy during Macrophage Infection byInternational journal of molecular sciences · 2024
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  12. Article
  13. Review
  14. Interleukin-10 Family and Tuberculosis: An Old Story Renewed.International journal of biological sciences · 2016
    Review
  15. Article
  16. 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

9 authors at 2 institutions in 1 country.

Shibali DasDivision of Molecular Medicine, Bose Institute, Kolkata, India.
Sayantan BanerjeeDivision of Molecular Medicine, Bose Institute, Kolkata, India.
Saikat MajumderDivision of Molecular Medicine, Bose Institute, Kolkata, India.
Bidisha Paul ChowdhuryDivision of Molecular Medicine, Bose Institute, Kolkata, India.
Avranil GoswamiDepartment of Microbiology, Institute of Post Graduate Medical Education and Research, Kolkata, India.
Kuntal HalderDivision of Molecular Medicine, Bose Institute, Kolkata, India.
Urmita ChakrabortyDepartment of Microbiology, Institute of Post Graduate Medical Education and Research, Kolkata, India.
Nishith K PalDepartment of Microbiology, Institute of Post Graduate Medical Education and Research, Kolkata, India; Department of Microbiology, Malda Medical College, Malda, India.
Subrata MajumdarDivision of Molecular Medicine, Bose Institute, Kolkata, India.
Bose Institute · INInstitute of Post Graduate Medical Education and Research · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tuberculosis is characterized by severe immunosuppression of the host macrophages, resulting in the loss of the host protective immune responses. During Mycobacterium tuberculosis infection, the pathogen modulates C-C Chemokine Receptor 5 (CCR5) to enhance IL-10 production, indicating the possible involvement of CCR5 in regulation of the host immune response. Here, we found that Mycobacterium infection significantly increased CCR5 expression in macrophages there by facilitating the activation of its downstream signaling. These events culminated in up-regulation of the immunosuppressive cytokine IL-10 production, which was further associated with the down-regulation of macrophage MHC-II expression along with the up-regulation of CCR5 expression via engagement of STAT-3 in a positive feedback loop. Treatment of macrophages with CCR5 specific siRNA abrogated the IL-10 production and restored MHCII expression. While, in vivo CCR5 silencing was also effective for the restoration of host immune responses against tuberculosis. This study demonstrated that CCR5 played a very critical role for the immune subversion mechanism employed by the pathogen.

Indexed as

Immune EvasionAnimalsFemaleGene Expression RegulationHistocompatibility Antigens Class IIInterleukin-10MacrophagesMiceMice, Inbred BALB CMycobacterium tuberculosisReceptors, CCR5Signal TransductionSTAT3 Transcription FactorTuberculosisCCR5 protein, mouseHistocompatibility Antigens Class IIIL10 protein, mouseInterleukin-10Receptors, CCR5Stat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID24695099
PMCPMC3973661
OpenAlexW1979332019

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.