Evidence map›Paper›PMID 24711459›Full record

ArticleThe Journal of biological chemistry2014

Small molecule-directed immunotherapy against recurrent infection by Mycobacterium tuberculosis.

Debapriya Bhattacharya, Ved Prakash Dwivedi, Mamoudou Maiga, Mariama Maiga, Luc Van Kaer, William R Bishai, Gobardhan Das

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 42 citations in OpenAlex.

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  11. The Human Microbiome in the Fight Against Tuberculosis.The American journal of tropical medicine and hygiene · 2017
    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

7 authors at 3 institutions in 2 countries.

Debapriya BhattacharyaFrom the Laboratory Medicine and Medical Sciences, College of Health Sciences, University of Kwazulu Natal, Durban 4001, South Africa.
Ved Prakash DwivediFrom the Laboratory Medicine and Medical Sciences, College of Health Sciences, University of Kwazulu Natal, Durban 4001, South Africa.
Mamoudou Maigathe Center for Tuberculosis Research, Department of Medicine, The Johns Hopkins University, Baltimore, Maryland 21231-1001, and.
Mariama Maigathe Center for Tuberculosis Research, Department of Medicine, The Johns Hopkins University, Baltimore, Maryland 21231-1001, and.
Luc Van Kaerthe Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232.
William R Bishaithe Center for Tuberculosis Research, Department of Medicine, The Johns Hopkins University, Baltimore, Maryland 21231-1001, and.
Gobardhan DasFrom the Laboratory Medicine and Medical Sciences, College of Health Sciences, University of Kwazulu Natal, Durban 4001, South Africa, gobardhan.das07@gmail.com.
Johns Hopkins University · USUniversity of KwaZulu-Natal · ZAVanderbilt University · US

Funding

Wellcome Trust
6 · The paper itself

Abstract

Tuberculosis remains the biggest infectious threat to humanity with one-third of the population infected and 1.4 million deaths and 8.7 million new cases annually. Current tuberculosis therapy is lengthy and consists of multiple antimicrobials, which causes poor compliance and high treatment dropout, resulting in the development of drug-resistant variants of tuberculosis. Therefore, alternate methods to treat tuberculosis are urgently needed. Mycobacterium tuberculosis evades host immune responses by inducing T helper (Th)2 and regulatory T (Treg) cell responses, which diminish protective Th1 responses. Here, we show that animals (Stat-6(-/-)CD4-TGFβRIIDN mice) that are unable to generate both Th2 cells and Tregs are highly resistant to M. tuberculosis infection. Furthermore, simultaneous inhibition of these two subsets of Th cells by therapeutic compounds dramatically reduced bacterial burden in different organs. This treatment was associated with the generation of protective Th1 immune responses. As these therapeutic agents are not directed to the harbored organisms, they should avoid the risk of promoting the development of drug-resistant M. tuberculosis variants.

Indexed as

ImmunotherapyAnimalsFlow CytometryMiceMice, Inbred BALB CMycobacterium tuberculosisTh1 CellsTh2 CellsTuberculosisImmunologyImmunotherapyInterleukinMycobacterium tuberculosisT Cell

Identifiers

PMID24711459
PMCPMC4047417
OpenAlexW2048140313

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.