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JSP1 Regulates Neutrophil Adhesion via Integrin-SRC Signaling in Vascular Inflammation
Biorxiv : the Preprint Server for Biology
|September 15, 2025
Summary
c-JUN N-terminal kinase (JNK)-stimulatory phosphatase 1 (JSP1) is crucial for neutrophil-driven vascular inflammation. JSP1 deficiency in mice reduces vascular injury and hemorrhage during innate immune responses.
Area of Science:
- Immunology
- Molecular Biology
- Cell Biology
Background:
- The c-JUN N-terminal kinase (JNK) pathway regulates innate immunity.
- Protein phosphatases balance kinase activity but are less understood.
- JSP1 (DUSP22) is a JNK-stimulatory phosphatase with an unclear role in innate immunity.
Purpose of the Study:
- To investigate the role of JSP1 in innate immunity and neutrophil-mediated vascular inflammation.
- To elucidate the mechanism by which JSP1 regulates neutrophil function.
Main Methods:
- Mouse model of the local Shwartzman reaction.
- JSP1-deficient mice and wild-type littermates.
- Neutrophil depletion and adoptive transfer experiments.
- Analysis of neutrophil integrin activation, adhesion, and signaling.
Main Results:
- JSP1 is essential for LPS-TNFα-induced vascular injury.
- JSP1-deficient mice show reduced vascular hemorrhage.
- JSP1-expressing neutrophils mediate vascular injury.
- JSP1 is critical for neutrophil integrin activation and adhesion.
- JSP1 deficiency impairs SYK and HCK phosphorylation in neutrophils.
Conclusions:
- JSP1 is a key regulator of neutrophil-driven vascular inflammation.
- JSP1 controls neutrophil adhesion and migration through integrin-SRC signaling.
- Targeting JSP1 may offer therapeutic strategies for inflammatory diseases.
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