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Related Experiment Video

Updated: May 29, 2025

A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry

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Published on: June 5, 2019

A GPVI-platelet-neutrophil-NET axis drives systemic sclerosis.

Roxane Darbousset, Leetah Senkpeil, Julia Kuehn

Biorxiv : the Preprint Server for Biology

|February 3, 2025

Summary

This summary is machine-generated.

Systemic sclerosis (SSc) involves neutrophil activation, leading to fibrosis. Platelets and neutrophil extracellular traps (NETs) are key drivers, revealing a GPVI-platelet-neutrophil-NET axis for potential SSc therapies.

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Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease

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Last Updated: May 29, 2025

A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry

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Published on: June 5, 2019

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Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease

Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease

Published on: June 16, 2020

Area of Science:

Immunology
Rheumatology
Pathology

Background:

Systemic sclerosis (SSc) is a severe autoimmune disease with high mortality due to progressive organ fibrosis.
Current understanding of SSc pathogenesis, particularly the cellular mechanisms driving fibrosis, remains incomplete.

Purpose of the Study:

To elucidate the roles of neutrophils and platelets in SSc pathogenesis.
To identify key molecular pathways and effector mechanisms driving SSc fibrosis.
To explore potential therapeutic targets for SSc.

Main Methods:

Analysis of neutrophil and platelet activation in SSc patients and murine models.
Transcriptomic analysis of affected tissues.
Experimental models using neutrophil depletion, platelet depletion, and PAD4 knockout mice.
Adoptive transfer of neutrophils and platelets.
Assessment of neutrophil extracellular traps (NETs) and GPVI signaling.

Main Results:

Neutrophil activation is a hallmark of SSc, with SSc neutrophils inducing fibrosis in mice.
Platelet activation precedes and drives neutrophil activation and fibrosis.
Neutrophil extracellular traps (NETs) are essential effector mechanisms in SSc.
Platelet collagen receptor GPVI mediates platelet and neutrophil activation, crucial for SSc development.

Conclusions:

A novel GPVI-platelet-neutrophil-NET axis is identified as central to SSc pathogenesis.
Neutrophils, platelets, and NETs are necessary and sufficient for driving SSc fibrosis.
Targeting this axis, particularly GPVI, offers a promising therapeutic strategy for SSc.