Samuel Bertin
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Single-cell transcriptomics reveals immune remodeling of the murine lung microenvironment following chronic house dust mite exposure Open
Introduction House dust mite (HDM) is a common environmental aeroallergen strongly associated with asthma and chronic airway inflammation. While HDM exposure is known to induce T helper 2 (Th2)-mediated eosinophilic inflammation, its chron…
Multi-omics profiling reveals microenvironmental remodeling as a key driver of house dust mite-induced lung cancer progression Open
Summary Chronic exposure to the common aeroallergen house dust mite (HDM) induces lung inflammation and DNA damage, but its impact on lung cancer development remains largely unexplored. Using whole-genome sequencing, RNA-seq, and DNA methy…
View article: Supplementary Figure S8 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer
Supplementary Figure S8 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer Open
Supplementary Figure S8. The RORγ/γt inhibitors digoxin and SR2211 inhibit Th17 cell differentiation in vitro.
View article: Supplementary Figure S9 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer
Supplementary Figure S9 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer Open
Supplementary Figure S9. Gating strategies for the flow cytometry analysis of lymphoid cell populations.
View article: Supplementary Figure S7 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer
Supplementary Figure S7 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer Open
Supplementary Figure S7. Rorg expression is not increased in CSCs isolated from the lungs of KrasG12D mice.
View article: Supplementary Figure S12 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer
Supplementary Figure S12 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer Open
Supplementary Figure S12. Gating strategies for the flow cytometry analysis of myeloid cell populations.
View article: Supplementary Figure S13 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer
Supplementary Figure S13 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer Open
Supplementary Figure S13. Digoxin treatment does not alter the infiltration of M1, M2, or PD-1-expressing tumorassociated macrophages (TAMs) in the lungs of KrasG12D mice.
View article: Supplementary Table S3 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer
Supplementary Table S3 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer Open
Supplementary Table S3. Oligonucleotides used for qPCR analysis.
View article: Supplementary Figure S11 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer
Supplementary Figure S11 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer Open
Supplementary Figure S11. Digoxin treatment does not affect the infiltration of some of the major myeloid cell subsets into the lungs of KrasG12D mice.
View article: Supplementary Figure S1 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer
Supplementary Figure S1 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer Open
Supplementary Figure S1. Effect of digoxin treatment on tumor progression and cytokine expression in a KrasG12D-driven lung cancer (LC) model.
View article: Supplementary Figure S6 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer
Supplementary Figure S6 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer Open
Supplementary Figure S6. Rorg expression is not increased in LLC CSCs.
View article: Supplementary Table S1 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer
Supplementary Table S1 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer Open
Supplementary Table S1. Key resources table.
View article: Supplementary Figure S4 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer
Supplementary Figure S4 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer Open
Supplementary Figure S4. The proliferation and viability of LUAD cell lines are unaffected by RORγ/γt pharmacological inhibition or Rorc genetic deletion.
View article: Supplementary Figure S10 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer
Supplementary Figure S10 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer Open
Supplementary Figure S10. Digoxin treatment does not affect the infiltration of NK17, NKT17, and γ/δT17 cells into the lungs of KrasG12D mice.
View article: Supplementary Figure S2 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer
Supplementary Figure S2 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer Open
Supplementary Figure S2. mIF panel validation.
View article: Supplementary Figure S15 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer
Supplementary Figure S15 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer Open
Supplementary Figure S15. Effect of digoxin treatment on cytokine expression in urethane-treated Rag1–/– mice.
View article: Supplementary Figure S14 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer
Supplementary Figure S14 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer Open
Supplementary Figure S14. Effect of Rorc gene deletion in a urethane-induced LC model.
View article: Supplementary Figure S16 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer
Supplementary Figure S16 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer Open
Supplementary Figure S16. Analysis of IL17A, IL17F, and IL22 promotor methylation and gene expression in LUAD patients.
View article: Supplementary Table S2 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer
Supplementary Table S2 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer Open
Supplementary Table S2. Control and Rorc-targeting gRNA sequences and homology arm sequences used for CRISPR/Cas9 for Rorc KO and HDR repair.
View article: Supplementary Figure S5 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer
Supplementary Figure S5 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer Open
Supplementary Figure S5. Rorg expression is not regulated by IL-1R1 signaling in LC cells in vitro.
View article: Data from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer
Data from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer Open
The retinoic acid receptor–related orphan receptor C (RORC) gene encodes two isoforms, RORγ and RORγt, which function as transcription factors in different cell types. RORγt is expressed in specific immune cells involved in inflammatory re…
View article: Supplementary Figure S3 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer
Supplementary Figure S3 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer Open
Supplementary Figure S3. Pharmacological inhibition of RORγ/γt does not affect the expression of cell proliferation, cell death, or cell survival markers in a Kras-mutated mouse LC cell line.
View article: Supplementary Figure S17 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer
Supplementary Figure S17 from RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer Open
Supplementary Figure S17. Correlation between RORC gene expression and immune and stromal cell infiltration in LUAD patients.
Myeloid <span>cAMP</span> Reduction Shifts Rhinovirus‐Induced Airway Inflammation From Neutrophilic to Eosinophilic by Suppressing <span>M1</span> ‐Interstitial Macrophages Open
Background Asthma exacerbations caused by human rhinovirus (hRV) infection are characterized by airway neutrophilia and reduced corticosteroid response, leading to significant healthcare costs and lung function impairment. The Gαs subunit …
View article: RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer
RORγt Inhibition Reduces Protumor Inflammation and Decreases Tumor Growth in Experimental Models of Lung Cancer Open
The retinoic acid receptor–related orphan receptor C (RORC) gene encodes two isoforms, RORγ and RORγt, which function as transcription factors in different cell types. RORγt is expressed in specific immune cells involved in inflammatory re…
View article: In Vivo Bioluminescence Imaging of Tumor Progression in the Lewis Lung Carcinoma Orthotopic Mouse Model: A Comparison Between the Tail Vein Injection and Intranasal Instillation Methods
In Vivo Bioluminescence Imaging of Tumor Progression in the Lewis Lung Carcinoma Orthotopic Mouse Model: A Comparison Between the Tail Vein Injection and Intranasal Instillation Methods Open
Metastasis remains a leading cause of cancer‐related mortality, yet its study has been constrained by the lack of reliable animal models that faithfully replicate this complex process. Syngeneic models for studying lung cancer metastasis a…
Loss of cAMP Signaling in CD11c Immune Cells Protects Against Diet-Induced Obesity Open
In obesity, CD11c+ innate immune cells are recruited to adipose tissue and create an inflammatory state that causes both insulin and catecholamine resistance. We found that ablation of Gnas, the gene that encodes Gαs, in CD11c expressing c…
<strong>Loss of cAMP signaling in CD11c immune cells protects against diet-induced obesity</strong> Open
In obesity, CD11c+ innate immune cells are recruited to adipose tissue and create an inflammatory state that causes both insulin and catecholamine resistance. We found that ablation of Gnas, the gene that encodes Gas, in CD11c expressing c…
<strong>Loss of cAMP signaling in CD11c immune cells protects against diet-induced obesity</strong> Open
In obesity, CD11c+ innate immune cells are recruited to adipose tissue and create an inflammatory state that causes both insulin and catecholamine resistance. We found that ablation of Gnas, the gene that encodes Gas, in CD11c expressing c…