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Related Experiment Video

Updated: Jul 7, 2026

Stimulation of Vascular Endothelial Cells Using Neutrophil Extracellular Traps in the Presence of Low-Density Lipoprotein

Stimulation of Vascular Endothelial Cells Using Neutrophil Extracellular Traps in the Presence of Low-Density Lipoprotein

Published on: August 12, 2025

IL-7R-Enriched Extracellular Vesicles From the Thymus Drive Colitis via Promoting Neutrophil Extracellular Trap

Yao Liao^1,2,3, Yuheng Liu^1,2,3, Ruibing Yang^1,2,3

¹KingMed School of Laboratory Medicine, The Affiliated Traditional Chinese Medicine Hospital, Guangzhou Medical University, Guangzhou, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)

|July 6, 2026

Summary

Circulating extracellular vesicles (EVs) carrying interleukin-7 receptor (IL-7R) from the thymus worsen inflammatory bowel disease (IBD) by triggering neutrophil extracellular traps (NETs). Targeting this thymus-gut axis offers potential IBD therapies.

Keywords:

IL‐7R‐enriched extracellular vesicles inflammatory bowel disease neutrophil extracellular traps, thymus‐gut axis

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Published on: January 25, 2017

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Last Updated: Jul 7, 2026

Stimulation of Vascular Endothelial Cells Using Neutrophil Extracellular Traps in the Presence of Low-Density Lipoprotein

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Published on: August 12, 2025

Visualization of IL-22-expressing Lymphocytes Using Reporter Mice

Visualization of IL-22-expressing Lymphocytes Using Reporter Mice

Published on: January 25, 2017

Area of Science:

Immunology
Gastroenterology
Cell Biology

Background:

Inflammatory bowel disease (IBD) involves extra-intestinal organs, but gut-extraintestinal communication mechanisms are unclear.
Extracellular vesicles (EVs) are key mediators of inter-organ communication.
Neutrophil extracellular traps (NETs) contribute to IBD pathogenesis.

Purpose of the Study:

To elucidate the role of circulating EVs in IBD exacerbation.
To identify the specific molecular mechanisms driving gut-extraintestinal crosstalk in IBD.
To investigate the thymus-gut axis in IBD pathogenesis.

Main Methods:

Investigated the effect of circulating EVs from colitis models on disease severity.
Analyzed EV cargo, focusing on interleukin-7 receptor (IL-7R) expression.
Examined the role of IL-7R and protein-arginine deiminase type 4 (PAD4) in NET formation.
Traced the origin of IL-7R-enriched EVs using thymus-gut axis models.

Main Results:

Circulating EVs from colitis exacerbate IBD by inducing NET formation.
EVs enriched with IL-7R are critical drivers of NET-mediated colitis.
IL-7R induces NETs via the PAD4 pathway, worsening colitis.
Thymus-derived EVs are the primary source of IL-7R-enriched EVs during colitis, stimulated by lipopolysaccharide (LPS).

Conclusions:

A novel thymus-gut communication axis mediated by IL-7R-enriched EVs exacerbates IBD.
This pathway explains IBD prevalence in young adults and offers potential therapeutic targets.
Inhibition of this axis may represent a new strategy for IBD management.