Greater Boston
My research has focused on understanding how synthetic biomaterials interact with immune cells and tissue, specifically focusing on the molecular mechanism of foreign body response (FBR). Macrophages and the innate immune response are considered central to the FBR and implant fibrosis, however, since the innate and adaptive immune systems are intimately connected, it is possible that the adaptive immune system is also contributing to the FBR. Implantation of a biomaterial or clinical devices may therefore impact immune memory and systemic immune responses with yet unexplored clinical consequences. Here, we demonstrated that the adaptive T cells and cellular senescence regulate the inflammatory response associated with biomaterial implant. We found that the induction and maintenance of pro-fibrotic IL-17 were associated with fibrotic progression and senescence development. Hence, blockage of type 17 signaling and/or removal of senescent cells by Navitoclax ameliorated fibrosis associated with FBR.