Sang Hun Lee, Ph.D.

Macrophages are considered a critical component of innate immunity against intracellular pathogens. Although macrophages have historically been viewed as monocyte-derived and terminally differentiated cells, recent progress has revealed that many tissue-resident macrophages are embryonically seeded, self-renewed, and perform homeostatic functions associated with M2-like activation programs. There is evidence that tissue-resident macrophages (TRMs) maintain their M2-like phenotype even in an infection-driven pro-inflammatory environment. In this regard, several intracellular pathogens, such as leishmania, are shown to exploit M2-like TRMs as replicative niches to evade pathogen-specific immunity.

Dr. Lee’s primary interests are understanding how the localized circuitries between various neuronal and immune cells, such as sensory neurons, innate lymphoid cells, and eosinophils, allow dermis resident macrophages to maintain M2-like properties and provide replicative niches for parasite growth even in a strong pro-inflammatory environment. This knowledge provides a new perspective to understand the chronicity of infections and develop therapeutic strategies which can selectively target TRMs.