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Article ; Online: Psoriasis Caught in the NET.

Di Domizio, Jeremy / Gilliet, Michel

The Journal of investigative dermatology

2019 Volume 139, Issue 7, Page(s) 1426–1429

Abstract: A report in the June 2019 issue of the Journal of Investigative Dermatology reveals a role of neutrophil extracellular traps (NETs) in the induction of T helper type 17 cell responses and shows the relevance of this pathway in patients with psoriasis ... ...

Abstract	A report in the June 2019 issue of the Journal of Investigative Dermatology reveals a role of neutrophil extracellular traps (NETs) in the induction of T helper type 17 cell responses and shows the relevance of this pathway in patients with psoriasis carrying a common risk variant in the TRAF3IP2 gene (Lambert et al., 2019). This work provides a new piece to the puzzle that links neutrophils to the T helper type 17-mediated pathogenesis of psoriasis.
MeSH term(s)	Adaptor Proteins, Signal Transducing ; Extracellular Traps ; Genotype ; Humans ; Neutrophils ; Psoriasis ; Th17 Cells ; Tumor Necrosis Factor Receptor-Associated Peptides and Proteins
Chemical Substances	Adaptor Proteins, Signal Transducing ; TRAF3IP2 protein, human ; Tumor Necrosis Factor Receptor-Associated Peptides and Proteins
Language	English
Publishing date	2019-06-24
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	80136-7
ISSN	1523-1747 ; 0022-202X
ISSN (online)	1523-1747
ISSN	0022-202X
DOI	10.1016/j.jid.2019.04.020
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Article ; Online: Human neutrophils drive skin autoinflammation by releasing interleukin (IL)-26.

Baldo, Alessia / Di Domizio, Jeremy / Yatim, Ahmad / Vandenberghe-Dürr, Sophie / Jenelten, Raphael / Fries, Anissa / Grizzetti, Lorenzo / Kuonen, François / Paul, Carle / Modlin, Robert L / Conrad, Curdin / Gilliet, Michel

The Journal of experimental medicine

2024 Volume 221, Issue 5

Abstract: Autoinflammation is a sterile inflammatory process resulting from increased neutrophil infiltration and overexpression of IL-1 cytokines. The factors that trigger these events are, however, poorly understood. By investigating pustular forms of psoriasis, ...

Abstract	Autoinflammation is a sterile inflammatory process resulting from increased neutrophil infiltration and overexpression of IL-1 cytokines. The factors that trigger these events are, however, poorly understood. By investigating pustular forms of psoriasis, we show that human neutrophils constitutively express IL-26 and abundantly release it from granular stores upon activation. In pustular psoriasis, neutrophil-derived IL-26 drives the pathogenic autoinflammation process by inducing the expression of IL-1 cytokines and chemokines that further recruit neutrophils. This occurs via activation of IL-26R in keratinocytes and via the formation of complexes between IL-26 and microbiota DNA, which trigger TLR9 activation of neutrophils. Thus our findings identify neutrophils as an important source of IL-26 and point to IL-26 as the key link between neutrophils and a self-sustaining autoinflammation loop in pustular psoriasis.
MeSH term(s)	Humans ; Neutrophils ; Psoriasis ; Interleukins ; Cytokines ; Interleukin-1
Chemical Substances	Interleukins ; Cytokines ; Interleukin-1
Language	English
Publishing date	2024-03-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20231464
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Ua VI Zs.107: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Activin A-Mediated Polarization of Cancer-Associated Fibroblasts and Macrophages Confers Resistance to Checkpoint Immunotherapy in Skin Cancer.

Pich-Bavastro, Christine / Yerly, Laura / Di Domizio, Jeremy / Tissot-Renaud, Stéphanie / Gilliet, Michel / Kuonen, François

Clinical cancer research : an official journal of the American Association for Cancer Research

2023 Volume 29, Issue 17, Page(s) 3498–3513

Abstract: Purpose: Cemiplimab is approved for the treatment of locally advanced basal cell carcinomas (BCC), although with mitigated results. We sought to interrogate the cellular and molecular transcriptional reprogramming underlying BCC resistance to ... ...

Abstract	Purpose: Cemiplimab is approved for the treatment of locally advanced basal cell carcinomas (BCC), although with mitigated results. We sought to interrogate the cellular and molecular transcriptional reprogramming underlying BCC resistance to immunotherapy. Experimental design: Here, we combined spatial and single-cell transcriptomics to deconvolute the spatial heterogeneity of the tumor microenvironment in regard with response to immunotherapy, in a cohort of both naïve and resistant BCCs. Results: We identified subsets of intermingled cancer-associated fibroblasts (CAF) and macrophages contributing the most to CD8 T-cell exclusion and immunosuppression. Within this spatially resolved peritumoral immunosuppressive niche, CAFs and adjacent macrophages were found to display Activin A-mediated transcriptional reprogramming towards extracellular matrix remodeling, suggesting active participation to CD8 T-cell exclusion. In independent datasets of human skin cancers, Activin A-conditioned CAFs and macrophages were associated with resistance to immune checkpoint inhibitors (ICI). Conclusions: Altogether, our data identify the cellular and molecular plasticity of tumor microenvironment (TME) and the pivotal role of Activin A in polarizing the TME towards immune suppression and ICI resistance.
MeSH term(s)	Humans ; Cancer-Associated Fibroblasts/pathology ; Skin Neoplasms/drug therapy ; Skin Neoplasms/genetics ; Carcinoma, Basal Cell/pathology ; Macrophages/pathology ; Immunotherapy ; Tumor Microenvironment
Chemical Substances	activin A
Language	English
Publishing date	2023-06-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-23-0219
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Article ; Online: SYNTHETIC BIOLOGY. Designer cells finely tuned for therapy.

Di Domizio, Jeremy / Gilliet, Michel

Science (New York, N.Y.)

2015 Volume 350, Issue 6267, Page(s) 1478–1479

MeSH term(s)	Designer Drugs ; Genetic Engineering ; Humans ; Synthetic Biology
Chemical Substances	Designer Drugs
Language	English
Publishing date	2015-12-18
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.aad9464
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Zs.A 27: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Xenotransplantation Model of Psoriasis.

Di Domizio, Jeremy / Conrad, Curdin / Gilliet, Michel

Methods in molecular biology (Clifton, N.J.)

2017 Volume 1559, Page(s) 83–90

Abstract: Psoriasis is a chronic autoimmune skin disease affecting approximately 2 % of the population with a major psychosocial and socioeconomic impact. A causal therapy leading to permanent cure is not available, and current treatments only lead to limited ... ...

Abstract	Psoriasis is a chronic autoimmune skin disease affecting approximately 2 % of the population with a major psychosocial and socioeconomic impact. A causal therapy leading to permanent cure is not available, and current treatments only lead to limited amelioration, and therefore new therapeutic targets need to be identified. Recent works demonstrated a predominant role of T
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-6786-5_7
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Article ; Online: Type I IFNs link skin-associated dysbiotic commensal bacteria to pathogenic inflammation and angiogenesis in rosacea.

Mylonas, Alessio / Hawerkamp, Heike C / Wang, Yichen / Chen, Jiaqi / Messina, Francesco / Demaria, Olivier / Meller, Stephan / Homey, Bernhard / Di Domizio, Jeremy / Mazzolai, Lucia / Hovnanian, Alain / Gilliet, Michel / Conrad, Curdin

JCI insight

2023 Volume 8, Issue 4

Abstract: Rosacea is a common chronic inflammatory skin disease with a fluctuating course of excessive inflammation and apparent neovascularization. Microbial dysbiosis with a high density of Bacillus oleronius and increased activity of kallikrein 5, which cleaves ...

Abstract	Rosacea is a common chronic inflammatory skin disease with a fluctuating course of excessive inflammation and apparent neovascularization. Microbial dysbiosis with a high density of Bacillus oleronius and increased activity of kallikrein 5, which cleaves cathelicidin antimicrobial peptide, are key pathogenic triggers in rosacea. However, how these events are linked to the disease remains unknown. Here, we show that type I IFNs produced by plasmacytoid DCs represent the pivotal link between dysbiosis, the aberrant immune response, and neovascularization. Compared with other commensal bacteria, B. oleronius is highly susceptible and preferentially killed by cathelicidin antimicrobial peptides, leading to enhanced generation of complexes with bacterial DNA. These bacterial DNA complexes but not DNA complexes derived from host cells are required for cathelicidin-induced activation of plasmacytoid DCs and type I IFN production. Moreover, kallikrein 5 cleaves cathelicidin into peptides with heightened DNA binding and type I IFN-inducing capacities. In turn, excessive type I IFN expression drives neoangiogenesis via IL-22 induction and upregulation of the IL-22 receptor on endothelial cells. These findings unravel a potentially novel pathomechanism that directly links hallmarks of rosacea to the killing of dysbiotic commensal bacteria with induction of a pathogenic type I IFN-driven and IL-22-mediated angiogenesis.
MeSH term(s)	Humans ; Bacteria ; Cathelicidins ; DNA, Bacterial ; Dysbiosis/microbiology ; Endothelial Cells/metabolism ; Inflammation/metabolism ; Inflammation/microbiology ; Kallikreins ; Rosacea/metabolism ; Rosacea/microbiology ; Rosacea/pathology ; Interferon Type I/metabolism ; Microbiota/physiology ; Bacillus/metabolism ; Skin/metabolism ; Skin/microbiology ; Skin/pathology ; Neovascularization, Pathologic/microbiology
Chemical Substances	Cathelicidins ; DNA, Bacterial ; Kallikreins (EC 3.4.21.-) ; Interferon Type I
Language	English
Publishing date	2023-02-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.151846
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Article ; Online: Differentiation of IL-26

Fries, Anissa / Saidoune, Fanny / Kuonen, François / Dupanloup, Isabelle / Fournier, Nadine / Guerra de Souza, Ana Cristina / Haniffa, Muzlifah / Ma, Feiyang / Gudjonsson, Johann E / Roesner, Lennart / Li, Yang / Werfel, Thomas / Conrad, Curdin / Gottardo, Raphael / Modlin, Robert L / Di Domizio, Jeremy / Gilliet, Michel

Nature communications

2023 Volume 14, Issue 1, Page(s) 3878

Abstract: Interleukin (IL)-26 is a ... ...

Abstract	Interleukin (IL)-26 is a T
MeSH term(s)	Humans ; Transforming Growth Factor beta1 ; Interleukin-17/genetics ; Cell Differentiation ; Psoriasis ; Skin
Chemical Substances	Transforming Growth Factor beta1 ; Interleukin-17
Language	English
Publishing date	2023-06-30
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-39484-4
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Article ; Online: Fueling autoimmunity: type I interferon in autoimmune diseases.

Di Domizio, Jeremy / Cao, Wei

Expert review of clinical immunology

2013 Volume 9, Issue 3, Page(s) 201–210

Abstract: In recent years, active research using genomic, cellular and animal modeling approaches has revealed the fundamental forces driving the development of autoimmune diseases. Type I interferon imprints unique molecular signatures in a list of autoimmune ... ...

Abstract	In recent years, active research using genomic, cellular and animal modeling approaches has revealed the fundamental forces driving the development of autoimmune diseases. Type I interferon imprints unique molecular signatures in a list of autoimmune diseases. Interferon is induced by diverse nucleic acid-containing complexes, which trigger innate immune activation of plasmacytoid dendritic cells. Interferon primes, activates or differentiates various leukocyte populations to promote autoimmunity. Accordingly, interferon signaling is essential for the initiation and/or progression of lupus in several experimental models. However, the heterogeneous nature of systemic lupus erythematosus requires better characterization on how interferon pathways are activated and subsequently promote the advancement of autoimmune diseases. Given the central role of type I interferon, various strategies are devised to target these cytokines or related pathways to curtail the progression of autoimmune diseases.
MeSH term(s)	Autoimmune Diseases/immunology ; Autoimmune Diseases/physiopathology ; Autoimmunity/immunology ; Dendritic Cells/immunology ; Humans ; Immunity, Innate/immunology ; Interferon Type I/immunology ; Lupus Erythematosus, Systemic/immunology
Chemical Substances	Interferon Type I
Language	English
Publishing date	2013-02-27
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2274260-8
ISSN	1744-8409 ; 1744-666X
ISSN (online)	1744-8409
ISSN	1744-666X
DOI	10.1586/eci.12.106
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Zs.A 6661: Show issues

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Article ; Online: Type I IFNs link skin-associated dysbiotic commensal bacteria to pathogenic inflammation and angiogenesis in rosacea

Alessio Mylonas / Heike C. Hawerkamp / Yichen Wang / Jiaqi Chen / Francesco Messina / Olivier Demaria / Stephan Meller / Bernhard Homey / Jeremy Di Domizio / Lucia Mazzolai / Alain Hovnanian / Michel Gilliet / Curdin Conrad

JCI Insight, Vol 8, Iss

2023 Volume 4

Abstract	Rosacea is a common chronic inflammatory skin disease with a fluctuating course of excessive inflammation and apparent neovascularization. Microbial dysbiosis with a high density of Bacillus oleronius and increased activity of kallikrein 5, which cleaves cathelicidin antimicrobial peptide, are key pathogenic triggers in rosacea. However, how these events are linked to the disease remains unknown. Here, we show that type I IFNs produced by plasmacytoid DCs represent the pivotal link between dysbiosis, the aberrant immune response, and neovascularization. Compared with other commensal bacteria, B. oleronius is highly susceptible and preferentially killed by cathelicidin antimicrobial peptides, leading to enhanced generation of complexes with bacterial DNA. These bacterial DNA complexes but not DNA complexes derived from host cells are required for cathelicidin-induced activation of plasmacytoid DCs and type I IFN production. Moreover, kallikrein 5 cleaves cathelicidin into peptides with heightened DNA binding and type I IFN–inducing capacities. In turn, excessive type I IFN expression drives neoangiogenesis via IL-22 induction and upregulation of the IL-22 receptor on endothelial cells. These findings unravel a potentially novel pathomechanism that directly links hallmarks of rosacea to the killing of dysbiotic commensal bacteria with induction of a pathogenic type I IFN–driven and IL-22–mediated angiogenesis.
Keywords	Dermatology ; Inflammation ; Medicine ; R
Language	English
Publishing date	2023-02-01T00:00:00Z
Publisher	American Society for Clinical investigation
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Integrated multi-omics reveals cellular and molecular interactions governing the invasive niche of basal cell carcinoma.

Yerly, Laura / Pich-Bavastro, Christine / Di Domizio, Jeremy / Wyss, Tania / Tissot-Renaud, Stéphanie / Cangkrama, Michael / Gilliet, Michel / Werner, Sabine / Kuonen, François

Nature communications

2022 Volume 13, Issue 1, Page(s) 4897

Abstract: Tumors invade the surrounding tissues to progress, but the heterogeneity of cell types at the tumor-stroma interface and the complexity of their potential interactions hampered mechanistic insight required for efficient therapeutic targeting. Here, ... ...

Abstract	Tumors invade the surrounding tissues to progress, but the heterogeneity of cell types at the tumor-stroma interface and the complexity of their potential interactions hampered mechanistic insight required for efficient therapeutic targeting. Here, combining single-cell and spatial transcriptomics on human basal cell carcinomas, we define the cellular contributors of tumor progression. In the invasive niche, tumor cells exhibit a collective migration phenotype, characterized by the expression of cell-cell junction complexes. In physical proximity, we identify cancer-associated fibroblasts with extracellular matrix-remodeling features. Tumor cells strongly express the cytokine Activin A, and increased Activin A-induced gene signature is found in adjacent cancer-associated fibroblast subpopulations. Altogether, our data identify the cell populations and their transcriptional reprogramming contributing to the spatial organization of the basal cell carcinoma invasive niche. They also demonstrate the power of integrated spatial and single-cell multi-omics to decipher cancer-specific invasive properties and develop targeted therapies.
MeSH term(s)	Carcinoma, Basal Cell/pathology ; Cell Communication ; Extracellular Matrix/metabolism ; Fibroblasts/metabolism ; Humans ; Skin Neoplasms/pathology
Language	English
Publishing date	2022-08-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-32670-w
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