Project A10
Myeloid cell-regulatory T cell crosstalk in thrombus development and resolution
Background
Tissue injury induces a complex innate immune cell program, in which immune cells sense extracellular proteolytic activity through protease-activated receptors (PARs). Previously, we have shown that PAR signals control migration, polarization, and activity of monocytes and macrophages in tissue microenvironments to cause autoimmunity and tumor immune evasion.
We hypothesize that during tissue injury, PAR signaling controls the development of clot-resolving Treg cells.
Strategy
We employ PAR receptor knock-out and knock-in genetic mouse strains to evaluate the development, recruitment, and activation of tissue repair Treg cells. Further, we investigate the clot Treg-derived signals that lead to reprogramming of the myeloid compartment by analyzing the SPARC-Itgb1 axis.