Evidence map›Paper›PMID 32375053›Full record

ArticleCell reports2020

Suppression of Inflammasome Activation by IRF8 and IRF4 in cDCs Is Critical for T Cell Priming.

Margaret M McDaniel, Leah C Kottyan, Harinder Singh, Chandrashekhar Pasare

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 54 citations in OpenAlex.

  1. Interferon regulatory factors orchestrate CD8International journal of molecular medicine · 2026
    Review
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  4. The Immunogenic Role of Self-DNA in T Cell Immunity.Clinical reviews in allergy & immunology · 2025
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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

4 authors at 4 institutions in 1 country.

Margaret M McDanielImmunology Graduate Program, The University of Texas Southwestern Medical Center, Dallas, TX, USA; Division of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA; Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Leah C KottyanCenter for Autoimmune Genomics and Etiology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA; Department of Pediatrics, University of Cincinnati, College of Medicine, Cincinnati, OH, USA.
Harinder SinghCenter for Systems Immunology, Departments of Immunology and Computational and Systems Biology, University of Pittsburgh, Pittsburgh, PA, USA.
Chandrashekhar PasareDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA; Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA; Department of Pediatrics, University of Cincinnati, College of Medicine, Cincinnati, OH, USA. Electronic address: chandrashekhar.pasare@cchmc.org.
Cincinnati Children's Hospital Medical Center · USThe University of Texas Southwestern Medical Center · USUniversity of Cincinnati Medical Center · USUniversity of Pittsburgh · US

Funding

INTEGRATIVE IMMUNOLOGY TRAINING PROGRAMT32AI005284 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI Nan Yan · 2003 to 2026
$7.4M
Innate mechanisms of regulation of Th17 responsesR01AI123176 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI Chandrashekhar Pasare · 2017 to 2026
$4.4M
ROLE OF BCAP IN REGULATING INFLAMMATION AND ADAPTIVE IMMUNITYR01AI113125 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI PASARE, CHANDRASHEKHAR · 2015 to 2019
$1.8M
Endocytic Trafficking and Cell Signaling in Models of ARC SyndromeR01GM120196 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI KRAMER, HELMUT J · 2017 to 2020
$1.3M
NIAID NIH HHS R01 AI113125NIAID NIH HHS R01 AI123176NIAID NIH HHS T32 AI005284NIGMS NIH HHS R01 GM120196
6 · The paper itself

Abstract

Inflammasome activation leads to pyroptotic cell death, thereby eliminating the replicative niche of virulent pathogens. Although inflammasome-associated cytokines IL-1β and IL-18 have an established role in T cell function, whether inflammasome activation in dendritic cells (DCs) is critical for T cell priming is not clear. Here, we find that conventional DCs (cDCs) suppress inflammasome activation to prevent pyroptotic cell death, thus preserving their ability to prime both CD4 and CD8 T cells. Transcription factors IRF8 and IRF4, in cDC1s and cDC2s, respectively, mediate suppression of inflammasome activation by limiting the expression of inflammasome-associated genes. Overexpression of IRF4 or IRF8 inhibits inflammasome activation in macrophages, while reduced expression of IRF8 leads to aberrant inflammasome activation in cDC1s and hampers their ability to prime CD8 T cells. Thus, activation of inflammasome in DCs is detrimental to adaptive immunity, and our results reveal that cDCs use IRF4 and IRF8 to suppress this response.

Indexed as

Adaptive ImmunityAnimalsCD8-Positive T-LymphocytesDendritic CellsInflammasomesInterferon Regulatory Factor-4Interferon Regulatory Factor-8Interferon Regulatory FactorsMacrophagesInflammasomesInterferon Regulatory Factor-4Interferon Regulatory Factor-8Interferon Regulatory Factorsdendritic cellsIL-1βinflammasomeIRF4IRF8pyroptosisT cell primingvirulence factors

Identifiers

PMID32375053
PMCPMC7325595
OpenAlexW3021806665

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.