Article

Mitochondrial cyclophilin D promotes disease tolerance by licensing NK cell development and IL-22 production against influenza virus

2021-05-28

Abstract excerpt

<h4>ABSTRACT</h4> Immunity to infectious disease involves a combination of host resistance, which eliminates the pathogen, and disease tolerance, which limits tissue damage. While the severity of most pulmonary viral infections, including influenza A virus (IAV), is linked to excessive inflammation, our mechanistic understanding of this observation remains largely unknown. Here we show that mitochondrial cyclophi...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work: 4f7ed9cf-63e4-5818-9d4c-c992beb0d486
DOI: 10.1101/2021.05.28.445832

Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest

Mitochondrial cyclophilin D promotes disease tolerance by licensing NK cell development and IL-22 production against influenza virusDOI 10.1101/2021.05.28.445832Read

An Autoimmunity-associated allele of <i>PTPN22</i> enhances innate antiviral immunity to protect against acute coronavirus infectionSemantic proximity Read

Metabolic deficiencies underlie reduced plasmacytoid dendritic cell IFN-I production following viral infectionSemantic proximity Read

Systems genetics of influenza A virus-infected mice identifies TRIM21 as a critical regulator of pulmonary innate immune responseSemantic proximity Read

Mx1 reveals innate pathways to antiviral resistance and lethal influenza diseaseSemantic proximity Read

Acute Viral Respiratory Infection Rapidly Induces a CD8+ T Cell Exhaustion-like Phenotype.Semantic proximity Read

Potent NKT cell ligands overcome SARS-CoV-2 immune evasion to mitigate viral pathogenesis in mouse modelsSemantic proximity Read

IFNγ initiates TLR9-dependent autoimmune hepatitis in DNase II deficient miceSemantic proximity Read

Metabolic Deficiencies Underlie Plasmacytoid Dendritic Cell Exhaustion After Viral InfectionSemantic proximity Read

β-Glucan Reprograms Neutrophils to Induce Disease Tolerance Against Influenza A VirusSemantic proximity Read

Programmed Cell Death in the Pathogenesis of InfluenzaSemantic proximity Read

Toll-Interacting Protein in Pulmonary Diseases. Abiding by the Goldilocks PrincipleSemantic proximity Read

Neutrophil NADPH oxidase breaks the inflammatory IL-1β/IL-17A circuit to enhance pathogen clearance during respiratory virus infectionsSemantic proximity Read