Specialized regulatory T cells control venous blood clot resolution through SPARC

The cells and mechanisms involved in blood clot resorption are only partially known. We show that regulatory T cells (Tregs) accumulate in venous blood clots and regulate thrombolysis by controlling the recruitment, differentiation and matrix metalloproteinase (MMP) activity of monocytes. We describe a clot Treg population that forms the matricellular acid- and cysteine-rich protein SPARC (secreted protein acidic and rich in cysteine) and show that SPARC enhances monocyte MMP activity and that SPARC(+) Tregs are crucial for blood clot resorption. By comparing different treatment times, we define a therapeutic window of Treg expansion that accelerates clot resorption.

Automated summary

The cells and mechanisms involved in blood clot resorption are only partially known, with regulatory T cells playing a crucial role in regulating thrombolysis by controlling monocytes. The matricellular protein SPARC is shown to enhance monocyte activity and is crucial for blood clot resorption. Expanding Tregs within a therapeutic window can accelerate clot resorption.