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RESEARCH PRODUCT

Specialized regulatory T cells control venous blood clot resolution through SPARC.

Fatemeh ShahnehChristian BeckerAlexandra GrillTobias BoppKatrin SchäferMatthias KleinFelix FrauhammerVerena Raker

subject

0301 basic medicinemedicine.medical_treatmentImmunologyPopulation030204 cardiovascular system & hematologyMatrix metalloproteinaseBiochemistryT-Lymphocytes RegulatoryMonocytes03 medical and health sciences0302 clinical medicinemedicineAnimalsOsteonectinThrombuseducationVenous Thrombosiseducation.field_of_studyChemistryMonocyteFibrinolysisCell BiologyHematologyVenous bloodThrombolysismedicine.diseaseMatrix MetalloproteinasesResorptionCell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureCysteine

description

Abstract 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.

10.1182/blood.2020005407https://pubmed.ncbi.nlm.nih.gov/33734343