Bernhard Ryffel
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View article: Microbiota shape the colon epithelium controlling inter-crypt absorptive goblet cells via butyrate–GP R109A signalling
Microbiota shape the colon epithelium controlling inter-crypt absorptive goblet cells via butyrate–GP R109A signalling Open
The colonic epithelium is a key interface between the gut microbiota and the host. How microbiota-derived signals influence epithelial cell identity and function remains incompletely understood. Here, we used single-cell transcriptomics, a…
View article: The intrinsic expression of NLRP3 in Th17 cells promotes their protumor activity and conversion into Tregs
The intrinsic expression of NLRP3 in Th17 cells promotes their protumor activity and conversion into Tregs Open
View article: Ozone-induced lung injury and inflammation: Pathways and therapeutic targets for pulmonary diseases caused by air pollutants
Ozone-induced lung injury and inflammation: Pathways and therapeutic targets for pulmonary diseases caused by air pollutants Open
Exposure to ambient Ozone (O3) air pollution directly causes by its oxidative properties, respiratory epithelial cell injury, and cell death, which promote inflammation and hyperreactivity, posing a significant public health con…
View article: Maternal type 2 immunity promotes a microchimeric transfer of systemic type 2 immunity to offspring
Maternal type 2 immunity promotes a microchimeric transfer of systemic type 2 immunity to offspring Open
During maternity mothers undergo an immune pivot to a type 2 immune phenotype which is independent of any antigen experience. In this study we present this maternal Type 2 immunity as a key enabler of optimal maternally-driven microchimeri…
View article: The Chemokine System as a Key Regulator of Pulmonary Fibrosis: Converging Pathways in Human Idiopathic Pulmonary Fibrosis (IPF) and the Bleomycin-Induced Lung Fibrosis Model in Mice
The Chemokine System as a Key Regulator of Pulmonary Fibrosis: Converging Pathways in Human Idiopathic Pulmonary Fibrosis (IPF) and the Bleomycin-Induced Lung Fibrosis Model in Mice Open
Idiopathic pulmonary fibrosis (IPF) is a chronic and lethal interstitial lung disease (ILD) of unknown origin, characterized by limited treatment efficacy and a fibroproliferative nature. It is marked by excessive extracellular matrix depo…
View article: Opposite effects of systemic and local conditional CD11c+ myeloid cell depletion during bleomycin‐induced inflammation and fibrosis in mice
Opposite effects of systemic and local conditional CD11c+ myeloid cell depletion during bleomycin‐induced inflammation and fibrosis in mice Open
Rationale Elevated levels of CD11c+ myeloid cells are observed in various pulmonary disorders, including Idiopathic Pulmonary Fibrosis (IPF). Dendritic cells (DCs) and macrophages (MΦ) are critical antigen‐presenting cells (APCs) that dire…
View article: <scp>STING</scp> ‐dependent induction of neutrophilic asthma exacerbation in response to house dust mite
<span>STING</span> ‐dependent induction of neutrophilic asthma exacerbation in response to house dust mite Open
Background Severe refractory, neutrophilic asthma remains an unsolved clinical problem. STING agonists induce a neutrophilic response in the airways, suggesting that STING activation may contribute to the triggering of neutrophilic exacerb…
View article: Pulmonary Administration of TLR2/6 Agonist after Allergic Sensitization Inhibits Airway Hyper-Responsiveness and Recruits Natural Killer Cells in Lung Parenchyma
Pulmonary Administration of TLR2/6 Agonist after Allergic Sensitization Inhibits Airway Hyper-Responsiveness and Recruits Natural Killer Cells in Lung Parenchyma Open
Asthma is a chronic lung disease with persistent airway inflammation, bronchial hyper-reactivity, mucus overproduction, and airway remodeling. Antagonizing T2 responses by triggering the immune system with microbial components such as Toll…
View article: Editorial: Inflammasomes in human diseases and metabolism
Editorial: Inflammasomes in human diseases and metabolism Open
Citation: Mbalaviele G and Ryffel B (2024) Editorial: Inflammasomes in human diseases and metabolism. Front. Immunol. 15:1420303. doi: 10.3389/fimmu.2024.1420303
View article: A conserved transcriptional program for MAIT cells across mammalian evolution
A conserved transcriptional program for MAIT cells across mammalian evolution Open
Mucosal-associated invariant T (MAIT) cells harbor evolutionarily conserved TCRs, suggesting important functions. As human and mouse MAIT functional programs appear distinct, the evolutionarily conserved MAIT functional features remain uni…
View article: NLRP6 controls pulmonary inflammation from cigarette smoke in a gut microbiota-dependent manner
NLRP6 controls pulmonary inflammation from cigarette smoke in a gut microbiota-dependent manner Open
Chronic obstructive pulmonary disease (COPD) is a major health issue primarily caused by cigarette smoke (CS) and characterized by breathlessness and repeated airway inflammation. NLRP6 is a cytosolic innate receptor controlling intestinal…
View article: Editorial: Sepsis: studying the immune system to highlight biomarkers for diagnosis, prognosis and personalized treatments
Editorial: Sepsis: studying the immune system to highlight biomarkers for diagnosis, prognosis and personalized treatments Open
EDITORIAL article Front. Immunol., 22 November 2023Sec. Inflammation Volume 14 - 2023 | https://doi.org/10.3389/fimmu.2023.1325020
View article: Lung inflammation and interstitial fibrosis by targeted alveolar epithelial type I cell death
Lung inflammation and interstitial fibrosis by targeted alveolar epithelial type I cell death Open
Introduction The pathogenesis of chronic lung diseases is multifaceted with a major role of recurrent micro-injuries of the epithelium. While several reports clearly indicated a prominent role for surfactant-producing alveolar epithelial t…
View article: PLK1 inhibition dampens NLRP3 inflammasome–elicited response in inflammatory disease models
PLK1 inhibition dampens NLRP3 inflammasome–elicited response in inflammatory disease models Open
Unabated activation of the NLR family pyrin domain-containing 3 (NLRP3) inflammasome is linked with the pathogenesis of various inflammatory disorders. Polo-like kinase 1 (PLK1) has been widely studied for its role in mitosis. Here, using …
View article: mRNA 3’UTR lengthening by alternative polyadenylation attenuates inflammatory responses and correlates with virulence of Influenza A virus
mRNA 3’UTR lengthening by alternative polyadenylation attenuates inflammatory responses and correlates with virulence of Influenza A virus Open
Changes of mRNA 3’UTRs by alternative polyadenylation (APA) have been associated to numerous pathologies, but the mechanisms and consequences often remain enigmatic. By combining transcriptomics, proteomics and recombinant viruses we show …
View article: Data from Cancer Induces a Stress Ileopathy Depending on β-Adrenergic Receptors and Promoting Dysbiosis that Contributes to Carcinogenesis
Data from Cancer Induces a Stress Ileopathy Depending on β-Adrenergic Receptors and Promoting Dysbiosis that Contributes to Carcinogenesis Open
Gut dysbiosis has been associated with intestinal and extraintestinal malignancies, but whether and how carcinogenesis drives compositional shifts of the microbiome to its own benefit remains an open conundrum. Here, we show that malignant…
View article: Data from Cancer Induces a Stress Ileopathy Depending on β-Adrenergic Receptors and Promoting Dysbiosis that Contributes to Carcinogenesis
Data from Cancer Induces a Stress Ileopathy Depending on β-Adrenergic Receptors and Promoting Dysbiosis that Contributes to Carcinogenesis Open
Gut dysbiosis has been associated with intestinal and extraintestinal malignancies, but whether and how carcinogenesis drives compositional shifts of the microbiome to its own benefit remains an open conundrum. Here, we show that malignant…
View article: Supplementary Figure from Cancer Induces a Stress Ileopathy Depending on β-Adrenergic Receptors and Promoting Dysbiosis that Contributes to Carcinogenesis
Supplementary Figure from Cancer Induces a Stress Ileopathy Depending on β-Adrenergic Receptors and Promoting Dysbiosis that Contributes to Carcinogenesis Open
Supplementary Figure from Cancer Induces a Stress Ileopathy Depending on β-Adrenergic Receptors and Promoting Dysbiosis that Contributes to Carcinogenesis
View article: Supplementary Figure from Cancer Induces a Stress Ileopathy Depending on β-Adrenergic Receptors and Promoting Dysbiosis that Contributes to Carcinogenesis
Supplementary Figure from Cancer Induces a Stress Ileopathy Depending on β-Adrenergic Receptors and Promoting Dysbiosis that Contributes to Carcinogenesis Open
Supplementary Figure from Cancer Induces a Stress Ileopathy Depending on β-Adrenergic Receptors and Promoting Dysbiosis that Contributes to Carcinogenesis
View article: Supplementary Figure from Cancer Induces a Stress Ileopathy Depending on β-Adrenergic Receptors and Promoting Dysbiosis that Contributes to Carcinogenesis
Supplementary Figure from Cancer Induces a Stress Ileopathy Depending on β-Adrenergic Receptors and Promoting Dysbiosis that Contributes to Carcinogenesis Open
Supplementary Figure from Cancer Induces a Stress Ileopathy Depending on β-Adrenergic Receptors and Promoting Dysbiosis that Contributes to Carcinogenesis
View article: Supplementary Figure from Cancer Induces a Stress Ileopathy Depending on β-Adrenergic Receptors and Promoting Dysbiosis that Contributes to Carcinogenesis
Supplementary Figure from Cancer Induces a Stress Ileopathy Depending on β-Adrenergic Receptors and Promoting Dysbiosis that Contributes to Carcinogenesis Open
Supplementary Figure from Cancer Induces a Stress Ileopathy Depending on β-Adrenergic Receptors and Promoting Dysbiosis that Contributes to Carcinogenesis
View article: Supplementary Figure 2 from SOCS3 Transactivation by PPARγ Prevents IL-17–Driven Cancer Growth
Supplementary Figure 2 from SOCS3 Transactivation by PPARγ Prevents IL-17–Driven Cancer Growth Open
PDF file - 32K, DHA incorporates into splenic cells in vivo.
View article: Data from SOCS3 Transactivation by PPARγ Prevents IL-17–Driven Cancer Growth
Data from SOCS3 Transactivation by PPARγ Prevents IL-17–Driven Cancer Growth Open
Activation of the transcription factor PPARγ by the n-3 fatty acid docosahexaenoic acid (DHA) is implicated in controlling proinflammatory cytokine secretion, but the intracellular signaling pathways engaged by PPARγ are incompletely chara…
View article: Data from SOCS3 Transactivation by PPARγ Prevents IL-17–Driven Cancer Growth
Data from SOCS3 Transactivation by PPARγ Prevents IL-17–Driven Cancer Growth Open
Activation of the transcription factor PPARγ by the n-3 fatty acid docosahexaenoic acid (DHA) is implicated in controlling proinflammatory cytokine secretion, but the intracellular signaling pathways engaged by PPARγ are incompletely chara…
View article: Supplementary Figure Legend from SOCS3 Transactivation by PPARγ Prevents IL-17–Driven Cancer Growth
Supplementary Figure Legend from SOCS3 Transactivation by PPARγ Prevents IL-17–Driven Cancer Growth Open
PDF file - 93K
View article: Supplementary Figure Legend from SOCS3 Transactivation by PPARγ Prevents IL-17–Driven Cancer Growth
Supplementary Figure Legend from SOCS3 Transactivation by PPARγ Prevents IL-17–Driven Cancer Growth Open
PDF file - 93K
View article: Supplementary Figure 3 from SOCS3 Transactivation by PPARγ Prevents IL-17–Driven Cancer Growth
Supplementary Figure 3 from SOCS3 Transactivation by PPARγ Prevents IL-17–Driven Cancer Growth Open
PDF file - 50K, In vivo DHA treatment fails to prevent mammary cancer cell growth in vivo in absence of T cells.
View article: Supplementary Figure 4 from SOCS3 Transactivation by PPARγ Prevents IL-17–Driven Cancer Growth
Supplementary Figure 4 from SOCS3 Transactivation by PPARγ Prevents IL-17–Driven Cancer Growth Open
PDF file - 65K, IL-1β and IL-6 neutralization does not impair DHA in vivo effect on melanoma tumor outgrowth in competent mice.
View article: Supplementary Figure 3 from SOCS3 Transactivation by PPARγ Prevents IL-17–Driven Cancer Growth
Supplementary Figure 3 from SOCS3 Transactivation by PPARγ Prevents IL-17–Driven Cancer Growth Open
PDF file - 50K, In vivo DHA treatment fails to prevent mammary cancer cell growth in vivo in absence of T cells.
View article: Supplementary Figure 4 from SOCS3 Transactivation by PPARγ Prevents IL-17–Driven Cancer Growth
Supplementary Figure 4 from SOCS3 Transactivation by PPARγ Prevents IL-17–Driven Cancer Growth Open
PDF file - 65K, IL-1β and IL-6 neutralization does not impair DHA in vivo effect on melanoma tumor outgrowth in competent mice.