Elisa Gomez Perdiguero

Introduction

Within the hematopoietic system that produces all blood cells, tissue ‘resident’ macrophagesare a lineage of myeloid cells that arise from yolk sac-derived progenitors and that self-maintain in their tissue of residency, independently of adult hematopoietic stem cells (HSC).

Tissue ‘resident’ macrophages from the same lineage, such as liver Kupffer cells, brain microglia, epidermal Langerhans cells, lung alveolar macrophages…, display tissue-specific phenotypes, perform tissue-specific functions and have distinct gene expression profiles.Thus, resident macrophages are a unique system where the respective contributions of ontogeny and environment can be investigated.

Projects

Elisa Gomez Perdiguero’s lab will combine methods from the fields of immunology, developmental biology and angiogenesis to understand in vivo the development and lineage-specific function(s) of resident macrophages, thereby opening new venues of research into the interaction between macrophages and endothelial cells in response to tissue damage.

Projects in the lab aim to address the molecular mechanisms that control the development and specific functions of resident macrophages in tissue homeostasis and repair by using state-of-the-art genetic and developmental methods. Briefly, we aim to study:

1/ the molecular control of resident macrophage differentiation and self-renewal.

2/ the lineage-specific function(s) of resident macrophages during development, homeostasis and tissue repair.

3/ the crosstalk between resident macrophages and endothelial cells during development and tissue repair.

Impact

This project will open the way to unravel the respective contribution of ontogeny versus environment in macrophage proliferation and function(s). By studying macrophage biology from a developmental perspective, this project expose new opportunities to investigate whether self-renewal of fetal-derived (or ‘resident’) macrophage is maintained during aging or if such ‘resident’ fetal-derived macrophages are replaced over extended periods, as proposed for cardiac and lung macrophages. Exhaustion of their proliferative capacity could lead to their replacement by adult HSC-derived cells, thereby modifying tissue response to stress with age and thus open new horizons in the field of aging.