Evidence map›Paper›PMID 26048138›Full record

ArticleCell host & microbe2015

Mycobacterium tuberculosis Differentially Activates cGAS- and Inflammasome-Dependent Intracellular Immune Responses through ESX-1.

Ruth Wassermann, Muhammet F Gulen, Claudia Sala, Sonia Garcia Perin, Ye Lou, Jan Rybniker, Jonathan L Schmid-Burgk, Tobias Schmidt, Veit Hornung, Stewart T Cole and 1 more

Open access · bronzeAbstract readComment
PubMed Publisher
In one paragraph

Article in Cell host & microbe, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 266 papers.

0numbers the graph read from it
0cells of the map it votes in
266citing papers in PubMed
20.5field-weighted citation impact, top 1% 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

266 citing papers in PubMed, 390 citations in OpenAlex.

  1. Trial
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  12. CMPK2 restrictsbioRxiv : the preprint server for biology · 2026
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  15. Observational
  16. ThemBio · 2026
    Article
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206 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 2 countries.

Ruth WassermannGlobal Health Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland.
Muhammet F GulenGlobal Health Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland.
Claudia SalaGlobal Health Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland.
Sonia Garcia PerinGlobal Health Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland.
Ye LouGlobal Health Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland.
Jan RybnikerGlobal Health Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland; First Department of Internal Medicine, University of Cologne, 50937 Cologne, Germany.
Jonathan L Schmid-BurgkInstitute for Molecular Medicine, University Hospital, University of Bonn, 53127 Bonn, Germany.
Tobias SchmidtInstitute for Molecular Medicine, University Hospital, University of Bonn, 53127 Bonn, Germany.
Veit HornungInstitute for Molecular Medicine, University Hospital, University of Bonn, 53127 Bonn, Germany.
Stewart T ColeGlobal Health Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland. Electronic address: stewart.cole@epfl.ch.
Andrea AblasserGlobal Health Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland. Electronic address: andrea.ablasser@epfl.ch.
École Polytechnique Fédérale de Lausanne · CHUniversity of Bonn · DEUniversity of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cytosolic detection of microbial products is essential for the initiation of an innate immune response against intracellular pathogens such as Mycobacterium tuberculosis (Mtb). During Mtb infection of macrophages, activation of cytosolic surveillance pathways is dependent on the mycobacterial ESX-1 secretion system and leads to type I interferon (IFN) and interleukin-1β (IL-1β) production. Whereas the inflammasome regulates IL-1β secretion, the receptor(s) responsible for the activation of type I IFNs has remained elusive. We demonstrate that the cytosolic DNA sensor cyclic GMP-AMP synthase (cGAS) is essential for initiating an IFN response to Mtb infection. cGAS associates with Mtb DNA in the cytosol to stimulate cyclic GAMP (cGAMP) synthesis. Notably, activation of cGAS-dependent cytosolic host responses can be uncoupled from inflammasome activation by modulating the secretion of ESX-1 substrates. Our findings identify cGAS as an innate sensor of Mtb and provide insight into how ESX-1 controls the activation of specific intracellular recognition pathways.

Indexed as

AnimalsCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNA, BacterialFemaleHost-Pathogen InteractionsHumansInterferon Type IMaleMycobacterium tuberculosisNucleotidyltransferasesTuberculosiscGAS protein, humancGAS protein, mouseCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNA, BacterialInterferon Type INucleotidyltransferases

Identifiers

PMID26048138
OpenAlexW1798681852

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.