Phosphatidyl Inositol 3 Kinase-Gamma Balances Antiviral and Inflammatory Responses During Influenza A H1N1 Infection: From Murine Model to Genetic Association in Patients.

doi:10.3389/fimmu.2018.00975

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

Phosphatidyl Inositol 3 Kinase-Gamma Balances Antiviral and Inflammatory Responses During Influenza A H1N1 Infection: From Murine Model to Genetic Association in Patients.

Frontiers in immunology - 1 Jan 2018

Garcia Cristiana C, Tavares Luciana P, Dias Ana Carolina F, Kehdy Fernanda, Alvarado-Arnez Lucia Elena, Queiroz-Junior Celso M, Galvão Izabela, Lima Braulio H, Matos Aline R, Gonçalves Ana Paula F, Soriani Frederico M, Moraes Milton O, Marques João T, Siqueira Marilda M, Machado Alexandre M V, Sousa Lirlândia P, Russo Remo C, Teixeira Mauro M

Abstract excerpt

Influenza A virus (IAV) infection causes severe pulmonary disease characterized by intense leukocyte infiltration. Phosphoinositide-3 kinases (PI3Ks) are central signaling enzymes, involved in cell growth, survival, and migration. Class IB PI3K or phosphatidyl inositol 3 kinase-gamma (PI3Kγ), mainly expressed by leukocytes, is involved in cell migration during inflammation. Here, we investigated the contribution...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Antiviral Agents

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to CD8-Positive T-Lymphocytes

Share to Inflammation

Share to Influenza A Virus, H1N1 Subtype

Share to Influenza, Human

Share to MAP Kinase Signaling System

Share to Neutrophil Infiltration

Share to Orthomyxoviridae Infections

Source

Open in PubMed Open full text

Identifiers

PMID: 29867955
DOI: 10.3389/fimmu.2018.00975
PMCID: PMC5962662

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Phosphatidyl Inositol 3 Kinase-Gamma Balances Antiviral and Inflammatory Responses During Influenza A H1N1 Infection: From Murine Model to Genetic Association in Patients.PMID 29867955Read ↗

Ifitm3 limits the severity of acute influenza in mice.Semantic proximity Read ↗

IFITM3 restricts the morbidity and mortality associated with influenza.Semantic proximity Read ↗

IFITM3 restricts the morbidity and mortality associated with influenzaSemantic proximity Read ↗

Antiviral Protection by IFITM3 In VivoSemantic proximity Read ↗

IFITM3 protects the heart during influenza virus infectionSemantic proximity Read ↗

IFITM3 variants point to a critical role in emergent virus infections.Semantic proximity Read ↗

Implication of Inflammatory Macrophages, Nuclear Receptors, and Interferon Regulatory Factors in Increased Virulence of Pandemic 2009 H1N1 Influenza A Virus after Host AdaptationSemantic proximity Read ↗

Allergic airway reactions rewired by PI3Kδ mutation.Semantic proximity Read ↗

Unique and overlapping actions of Type I and III IFNs in influenza A virus infection and implications for therapySemantic proximity Read ↗

An updated systematic review of the role of host genetics in susceptibility to influenza.Semantic proximity Read ↗

Highly pathogenic avian influenza A H5N1 and pandemic H1N1 virus infections have different phenotypes in Toll-like receptor 3 knockout miceSemantic proximity Read ↗

Transcriptional analysis of immune-related gene expression in p53-deficient mice with increased susceptibility to influenza A virus infectionSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.