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Immune modules to guide diagnosis and personalized treatment of inflammatory skin diseases

Immune gene expression analysis can help differentiate between inflammatory skin diseases. Here the authors compare expression profiles between different human inflammatory skin diseases and identify gene modules such as cytokines or inflammatory mediators and a molecular map to assist in diagnosis and treatment.

Teofila Seremet
Jeremy Di Domizio
Michel Gilliet
ResearchOpen Access18 Dec 2024
Nature Communications

Volume: 15, P: 1-12
Differentiation of IL-26⁺ T_H17 intermediates into IL-17A producers via epithelial crosstalk in psoriasis

Interleukin 26 (IL-26) has been shown to have antimicrobial and pro-inflammatory effects. Here the authors establish a role for IL-26 in the generation of IL-17A producing Th17 CD4⁺ T cells and suggest it involves epithelial cross talk in skin lesions of psoriasis patients.

Anissa Fries
Fanny Saidoune
Michel Gilliet
ResearchOpen Access30 Jun 2023
Nature Communications

Volume: 14, P: 1-14
The cGAS–STING pathway drives type I IFN immunopathology in COVID-19

The cGAS–STING pathway has a central role in the pathogenesis of severe COVID-19 by driving the increase in type I interferons that occurs in the later stages of SARS-CoV-2 infection.

Jeremy Di Domizio
Muhammet F. Gulen
Andrea Ablasser
ResearchOpen Access19 Jan 2022
Nature

Volume: 603, P: 145-151
The commensal skin microbiota triggers type I IFN–dependent innate repair responses in injured skin

Gilliet and colleagues demonstrate that skin wound healing occurs through the coordinated action of plasmacytoid dendritic cells, chemokines and skin microbiota.

Jeremy Di Domizio
Cyrine Belkhodja
Michel Gilliet
Research13 Jul 2020
Nature Immunology

Volume: 21, P: 1034-1045
TNF blockade induces a dysregulated type I interferon response without autoimmunity in paradoxical psoriasis

The pathogenesis of paradoxical psoriasis in patients receiving anti-TNF treatments for classical psoriasis is unclear. Here, the authors show that anti-TNF drugs enhance the production of type I interferon by plasmacytoid dendritic cells, causing skin lesions that, unlike classical psoriasis, lack T- cell autoimmunity.

Curdin Conrad
Jeremy Di Domizio
Michel Gilliet
ResearchOpen Access02 Jan 2018
Nature Communications

Volume: 9, P: 1-11
T_H17 cells promote microbial killing and innate immune sensing of DNA via interleukin 26

T_H17 cells have important roles at mucosal surfaces in both health and disease. Gilliet and colleagues show that IL-26 is preferentially produced by human T_H17 cells and that this cytokine has both alarmin and direct antimicrobial functions.

Stephan Meller
Jeremy Di Domizio
Michel Gilliet
Research13 Jul 2015
Nature Immunology

Volume: 16, P: 970-979
Single cell and spatial sequencing define processes by which keratinocytes and fibroblasts amplify inflammatory responses in psoriasis

Changes in Psoriasis and other inflammatory skin diseases during severity stages can be investigated using single cell and spatial transcriptomics. Here the authors compare different inflammatory skin diseases to emphasise differences in immune cells and inflammatory markers particularly keratinocytes and fibroblasts.

Feiyang Ma
Olesya Plazyo
Johann E. Gudjonsson
ResearchOpen Access12 Jun 2023
Nature Communications

Volume: 14, P: 1-19
Integrated multi-omics reveals cellular and molecular interactions governing the invasive niche of basal cell carcinoma

The role of reciprocal tumour-stroma interactions in tumour invasion remains poorly characterised. Here, single-cell and spatial transcriptomics identifies the cell populations and their transcriptional reprogramming contributing to the spatial organization of the basal cell carcinoma invasive niche.

Laura Yerly
Christine Pich-Bavastro
François Kuonen
ResearchOpen Access20 Aug 2022
Nature Communications

Volume: 13, P: 1-16
Helical antimicrobial peptides assemble into protofibril scaffolds that present ordered dsDNA to TLR9

Amphihelical antimicrobial peptides (AMPs) are bactericidal host defense factors, but their function as immunomodulators is emerging. Here the authors show that several AMPs organize DNA into periodic nanocrystals by self-assembling into superhelical protofibril scaffolds, which potentiates DNA sensing by TLR9.

Ernest Y. Lee
Changsheng Zhang
Gerard C. L. Wong
ResearchOpen Access04 Mar 2019
Nature Communications

Volume: 10, P: 1-10
Diversification of human plasmacytoid predendritic cells in response to a single stimulus

Plasmacytoid dendritic cells (pDCs) are known for their copious IFN-I production. Soumelis and colleagues show that functionally and transcriptomically distinct human pDC populations can be generated from a single microbial or cytokine stimulus.

Solana G. Alculumbre
Violaine Saint-André
Vassili Soumelis
Research04 Dec 2017
Nature Immunology

Volume: 19, P: 63-75
Interleukin-26 activates macrophages and facilitates killing of Mycobacterium tuberculosis

Heike C. Hawerkamp
Lasse van Geelen
Stephan Meller
ResearchOpen Access14 Oct 2020
Scientific Reports

Volume: 10, P: 1-14

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Immune modules to guide diagnosis and personalized treatment of inflammatory skin diseases

Differentiation of IL-26⁺ T_H17 intermediates into IL-17A producers via epithelial crosstalk in psoriasis

The cGAS–STING pathway drives type I IFN immunopathology in COVID-19

The commensal skin microbiota triggers type I IFN–dependent innate repair responses in injured skin

TNF blockade induces a dysregulated type I interferon response without autoimmunity in paradoxical psoriasis

T_H17 cells promote microbial killing and innate immune sensing of DNA via interleukin 26

Single cell and spatial sequencing define processes by which keratinocytes and fibroblasts amplify inflammatory responses in psoriasis

Integrated multi-omics reveals cellular and molecular interactions governing the invasive niche of basal cell carcinoma

Helical antimicrobial peptides assemble into protofibril scaffolds that present ordered dsDNA to TLR9

Diversification of human plasmacytoid predendritic cells in response to a single stimulus

Interleukin-26 activates macrophages and facilitates killing of Mycobacterium tuberculosis

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