Evidence map›Paper›PMID 42600620›Full record

ArticleCell host & microbe2026

Strong, sustained type I IFN signaling acts cell intrinsically to impair IFNγ responses and cause tuberculosis susceptibility.

Stefan A Fattinger, Bianca Parisi, Roberto A Chavez, Marian R Fairgrieve, Ophelia V Lee, Kristen C Witt, Jesse J Rodriguez, Elizabeth A Turcotte, Ella C Brydon, Harmandeep Dhaliwal and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell host & microbe, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Diverse infection models demonstrate robust resistance ofbioRxiv : the preprint server for biology · 2026
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors.

Stefan A FattingerDivision of Immunology and Molecular Medicine, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA, USA. Electronic address: sfattinger@berkeley.edu.
Bianca ParisiDivision of Immunology and Molecular Medicine, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA, USA; Center for Emerging and Neglected Diseases, University of California, Berkeley, Berkeley, CA, USA.
Roberto A ChavezDivision of Immunology and Molecular Medicine, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA, USA; Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, CA, USA.
Marian R FairgrieveDivision of Immunology and Molecular Medicine, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA, USA; Center for Emerging and Neglected Diseases, University of California, Berkeley, Berkeley, CA, USA; Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, CA, USA.
Ophelia V LeeDivision of Immunology and Molecular Medicine, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA, USA.
Kristen C WittDivision of Immunology and Molecular Medicine, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA, USA.
Jesse J RodriguezDivision of Immunology and Molecular Medicine, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA, USA; Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, CA, USA.
Elizabeth A TurcotteDivision of Immunology and Molecular Medicine, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA, USA.
Ella C BrydonDivision of Immunology and Molecular Medicine, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA, USA; Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, CA, USA.
Harmandeep DhaliwalCancer Research Laboratory, University of California, Berkeley, Berkeley, CA, USA.
Angus Y LeeCancer Research Laboratory, University of California, Berkeley, Berkeley, CA, USA.
Dmitri I KotovDivision of Immunology and Molecular Medicine, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA, USA.
Russell E VanceDivision of Immunology and Molecular Medicine, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA, USA; Cancer Research Laboratory, University of California, Berkeley, Berkeley, CA, USA; Center for Emerging and Neglected Diseases, University of California, Berkeley, Berkeley, CA, USA; Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, CA, USA. Electronic address: rvance@berkeley.edu.

Funding

The role of Listeria cyclic-di-AMP during infection and immunityP01AI063302 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI PORTNOY, DANIEL A · 2004 to 2025
$45.5M
Functional and Structural Dissection of Inflammasome ActivationR37AI075039 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI RUSSELL E VANCE · 2018 to 2026
$3.8M
Specificity and in vivo function of the Naip/Nlrc4 inflammasomesR01AI075039 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI VANCE, RUSSELL E · 2008 to 2017
$3.6M
Dissection of Shigella pathogenesis in vivo using a new oral infection mouse modelR01AI155634 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI VANCE, RUSSELL E · 2020 to 2024
$2.2M
Howard Hughes Medical InstituteNIAID NIH HHS P01 AI063302NIAID NIH HHS R01 AI075039NIAID NIH HHS R01 AI155634NIAID NIH HHS R37 AI075039
6 · The paper itself

Abstract

Mycobacterium tuberculosis (Mtb) causes over one million deaths annually, but most infected individuals never exhibit symptoms. Type I interferons (IFNs) have emerged as a major factor driving susceptibility to Mtb, but how type I IFNs impair immunity to Mtb is a key unresolved question. Here, we show that an early effect of type I IFN during Mtb infection is the cell-intrinsic impairment of IFNγ signaling. IFNγ signaling is selectively impaired in the subset of infected macrophages experiencing high and sustained levels of type I IFN signaling. Genetic elimination of regulated stimulator of interferon via stabilization of transcript (RESIST), a recently described positive regulator of type I IFN production, specifically eliminates the high and sustained type I IFN response, fully restores IFNγ signaling, and rescues susceptibility to Mtb without affecting basal type I IFN responses. Our results demonstrate that strong and sustained type I IFN responses specifically and cell intrinsically impair responsiveness to IFNγ to cause susceptibility to Mtb.

Indexed as

Interferon-gammaInterferon Type IMycobacterium tuberculosisSignal TransductionTuberculosisAnimalsDisease SusceptibilityMacrophagesMiceMice, Inbred C57BLMice, KnockoutInterferon-gammaInterferon Type Iantibacterial immunityIFNγ responseimmunologyinterstitial macrophageslungmiceMycobacterium tuberculosistype I interferons

Identifiers

PMID42600620
PMCPMC13528601

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.