Identification and Functional Characterization of a New Thrombus-resolving Regulatory T-cell Population
ISTH Academy. Shahneh F. Jul 10, 2019; 273833; OC 77.5 Topic: Innate & Adaptive Immunity
Fatemeh Shahneh
Fatemeh Shahneh
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OC 77.5

Identification and Functional Characterization of a New Thrombus-resolving Regulatory T-cell Population

F. Shahneh1,2, M. Klein3, T. Bopp4, F. Marini1,5, A. Grill1, K. Schäfer6, C. Becker1,2
1University Medical Center Mainz, Johannes Gutenberg-University Mainz, Center for Thrombosis and Hemostasis, Mainz, Germany, 2University Medical Center Mainz, Johannes Gutenberg-University Mainz, Department of Dermatology, Mainz, Germany, 3University Medical Center Mainz, Johannes Gutenberg-University Mainz, Institute for Immunology, Mainz, Germany, 4University Medical Center Mainz, Johannes Gutenberg-University Mainz, Institute for Immunology, Mai, Germany, 5University Medical Center Mainz, Johannes Gutenberg-University Mainz, Institute of Medical Biostatistics, Epidemiology and Informatics (IMBEI), Mainz, Germany, 6University Medical Center Mainz, Johannes Gutenberg-University Mainz, Cardiology I, Mainz, Germany

Main Topic: Immunothrombosis and Vascular Biology
Category: Innate & Adaptive Immunity

Background: Deep vein thrombosis is associated with long-term complications, including venous thromboembolism, post-thrombotic syndrome and chronic thromboembolic pulmonary hypertension. CD4+Foxp3+ regulatory T (Treg) have a major direct and non-redundant role in tissue repair and maintenance, distinct from their role in suppression of immune responses. Whether and how Treg participate in thrombus resolution has not been investigated.
Aims: Based on the observation that Treg accumulate in venous thrombi, we aimed to clarify their functional role in venous clot resolution.
Methods: Experimental approaches included the selective manipulation of Treg numbers during thrombus resolution, comprehensive characterization of the histological and cellular changes induced by them, generation of Treg expression profiles and the identification of their clot-dissolving function at the molecular level.
Results: We describe a specialized population of resident 'clot-busting' Treg that develops in venous blood clots, is activated by monocyte-derived cytokines, and regulates thrombus resolution by imposing phenotypic and functional changes in the myeloid compartment.
Conclusions: Our study reveals a crucial role of specialized Treg in ordered blood clot resolution. Increasing Treg activity appears to be an attractive therapeutic approach for improving thrombus resolution and restoring organ function in chronic thromboinflammatory diseases. Treg-modulating reagents, that are already clinically tested, may be used for this purpose.

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