Our lab is investigating mechanisms of regulation of immune responses and tissue homeostasis by stromal cells, in particular in the context of inflammatory diseases and cancer.
Stromal cells are non-hematopoietic cells that support the structure and function of all our organs. In lymphoid organs, specialized subsets of stromal cells play a pivotal role in immune responses by producing chemokines and growth factors, which organize lymphocytes migration and survival, as well as interaction with other immune subsets. Stromal cells therefore are essential for the homeostasis of the immune system. Additionally, stromal cells play key roles in several biological processes including vascular remodeling, tissue repair/regeneration and inflammation.
Our lab is studying the crosstalk of specific subsets of stromal cells with immune cells, endothelial cells and tissue stem cells, and exploring how perturbation of this fundamental stromal crosstalk impact on disease pathogenesis. We, and others, have notably shown that stromal progenitors wrapped around vessels have an essential role in the scarring/fibrotic process, a major component of chronic diseases. We are using several experimental approaches, including cutting-edge lineage tracing and genetic depletion models for stromal subsets, cell imaging and transcriptomics.
A better knowledge of the stromal microenvironment is expected to improve our understanding of the biological processes underlying tissue repair and inflammation, paving the way for the discovery of new therapeutic approaches in chronic diseases where these processes become pathological, such as fibrotic diseases and cancer.
Our research is currently focusing on:
- Defining the role of lymphoid stromal cells in intestinal homeostasis and lymphoid organs
- Identifying perivascular stromal progenitors with roles in fibrosis and tissue regeneration
- Deciphering the stromal crosstalk to tumor cells and impact on tumor immunity and anti-cancer therapies
The stromal microenvironment of the intestinal lamina propria after prolonged inflammation of the digestive tract (colon) (Stzepourginski et al., PNAS 2017)
