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Related Experiment Video

Updated: May 20, 2026

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo

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Published on: July 20, 2019

TNFSF15 Modulates Neovascularization and Inflammation.

Zhisong Zhang¹, Lu-Yuan Li

¹College of Pharmacy, Nankai University, Tianjin, China.

Cancer Microenvironment : Official Journal of the International Cancer Microenvironment Society

|July 27, 2012

Summary

Tumor necrosis factor superfamily-15 (TNFSF15), also known as VEGI or TL1A, regulates vascular homeostasis and inflammation. This cytokine inhibits endothelial cell growth and stimulates immune responses, impacting angiogenesis and immune mobilization.

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Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response

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Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo

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Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response

Published on: September 15, 2017

Area of Science:

Immunology
Vascular Biology
Cytokine Signaling

Background:

Tumor necrosis factor superfamily-15 (TNFSF15), also known as VEGI or TL1A, is a cytokine involved in vascular homeostasis and inflammation.
TNFSF15 expression is high in mature vasculature but reduced in areas of neovascularization, such as tumors and wounds.

Purpose of the Study:

To review experimental evidence on the multifaceted roles of TNFSF15.
To elucidate TNFSF15's functions in angiogenesis, vasculogenesis, inflammation, and immune system modulation.

Main Methods:

Literature review of experimental studies on TNFSF15.
Analysis of TNFSF15's effects on endothelial cells, T cells, and dendritic cells.
Examination of TNFSF15's signaling pathways, including its interaction with death receptor-3.

Main Results:

TNFSF15 inhibits endothelial cell proliferation and differentiation of endothelial progenitor cells.
TNFSF15 promotes T cell activation, Th1 cytokine production, and dendritic cell maturation.
TNFSF15 plays a dual role in vascularization and immune responses.

Conclusions:

TNFSF15 is a key regulator of both vascular and immune processes.
Understanding TNFSF15's functions is crucial for developing therapies for cancer, inflammatory diseases, and wound healing.
Further research into TNFSF15 signaling pathways may reveal novel therapeutic targets.