Interleukin-17A Promotes Lung Tumor Progression through Neutrophil Attraction to Tumor Sites and Mediating Resistance to PD-1 Blockade.

doi:10.1016/j.jtho.2017.04.017

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

Interleukin-17A Promotes Lung Tumor Progression through Neutrophil Attraction to Tumor Sites and Mediating Resistance to PD-1 Blockade.

Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer - 1 Aug 2017

Akbay Esra A, Koyama Shohei, Liu Yan, Dries Ruben, Bufe Lauren E, Silkes Michael, Alam Md Maksudul, Magee Dillon M, Jones Robert, Jinushi Masahisa, Kulkarni Meghana, Carretero Julian, Wang Xiaoen, Warner-Hatten Tiquella, Cavanaugh Jillian D, Osa Akio, Kumanogoh Atsushi, Freeman Gordon J, Awad Mark M, Christiani David C, Bueno Raphael, Hammerman Peter S, Dranoff Glenn, Wong Kwok-Kin

Abstract excerpt

INTRODUCTION: Proinflammatory cytokine interleukin-17A (IL-17A) is overexpressed in a subset of patients with lung cancer. We hypothesized that IL-17A promotes a protumorigenic inflammatory phenotype and inhibits antitumor immune responses. METHODS: We generated bitransgenic mice expressing a conditional IL-17A allele along with conditional KrasG12D and performed immune phenotyping of mouse lungs, a survival...

Read the complete abstract on PubMed

Topics

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

Share to Disease Progression

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Expression

Share to Interleukin-17

Share to Lung Neoplasms

Share to Mice, Transgenic

Share to Neutrophils

Share to Programmed Cell Death 1 Receptor

Share to Proto-Oncogene Proteins p21(ras)

Source

Open in PubMed Open full text

Identifiers

PMID: 28483607
DOI: 10.1016/j.jtho.2017.04.017
PMCID: PMC5532066

Genes

EGF
KRAS

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Interleukin-17A Promotes Lung Tumor Progression through Neutrophil Attraction to Tumor Sites and Mediating Resistance to PD-1 Blockade.PMID 28483607Read ↗

T helper 17 cells play a critical pathogenic role in lung cancer.Semantic proximity Read ↗

STK11/LKB1 Deficiency Promotes Neutrophil Recruitment and Proinflammatory Cytokine Production to Suppress T-cell Activity in the Lung Tumor Microenvironment.Semantic proximity Read ↗

IL22 Promotes Kras-Mutant Lung Cancer by Induction of a Protumor Immune Response and Protection of Stemness Properties.Semantic proximity Read ↗

LIF-Induced Tumor Plasticity Establishes an Immunosuppressive Myeloid Niche in LKB1-Mutant Lung Cancer.Semantic proximity Read ↗

IL-17-producing γδ T cells and neutrophils conspire to promote breast cancer metastasis.Semantic proximity Read ↗

Targeting IL-1β as an immunopreventive and therapeutic modality for K-ras-mutant lung cancer.Semantic proximity Read ↗

Tumor-intrinsic LKB1-LIF signaling axis establishes a myeloid niche to promote immune evasion and tumor growthSemantic proximity Read ↗

Potential Impacts of Interleukin-17A Promoter Polymorphisms on the EGFR Mutation Status and Progression of Non-Small Cell Lung Cancer in Taiwan.Semantic proximity Read ↗

Macrophages, Inflammation, and Lung Cancer.Semantic proximity Read ↗

Lung adenocarcinoma–derived IFN-γ promotes growth by modulating CD8+ T cell production of CCR5 chemokinesSemantic proximity Read ↗

IL6 Blockade Reprograms the Lung Tumor Microenvironment to Limit the Development and Progression of K-ras-Mutant Lung Cancer.Semantic proximity Read ↗

Selective inhibition of canonical STAT3 signaling suppresses K-ras mutant lung tumorigenesis and reinvigorates anti-tumor immunity.Semantic proximity Read ↗

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