Abstract

We have been studying macrophage heterogeneity during inflammation and these studies have revealed that even in vascular tissues, tissue resident macrophages can be maintained as an independent self-renewing population of cells.

These cells are seeded into the tissue during development, expanded during the neonatal period and remarkably we found they were capable of remaining independent of bone marrow input during the recovery from inflammation. Proliferative renewal is not restricted to tissue resident macrophages as inflammatory bone marrow derived macrophages also proliferate during the resolution of inflammation. The autonomy of distinct macrophage lineages, within specific tissues, underscores the extensive heterogeneity of tissue resident macrophages, which is a necessary consequence of tissue and microanatomical niche specific functions. These discrete phenotypes must necessarily be dictated by specific transcriptional controls.

The identification of cell specific transcription factors and the consequences of their disruption will be discussed.