The Rothlin-Ghosh laboratory studies mechanisms that regulate the magnitude, quality, and duration of immune responses. While inflammation is essential for the initiation of adaptive immunity, its intensity and persistence must be tightly controlled to ensure effective host defense while preventing excessive or chronic responses causing collateral tissue damage. Work in the laboratory has uncovered a mechanism through which activated, but not resting, T cells signal to myeloid cells to suppress inflammatory cytokine production. Current efforts are focused on understanding naïve T cell heterogeneity and how distinct naïve T cell states can influence the intensity and quality of immune responses.
A major area of research in the laboratory centers on how sentinel cells sense tissue damage and cell death, and how these recognition pathways drive the resolution of inflammation to shape tissue repair programs. We have shown that coincidence detection of apoptotic neutrophils and IL-4 can induce macrophage tissue-repair responses. By contrast, the response to other forms of molecularly executed cell death can lead to distinct outcomes, such as continuing inflammation. Additionally, we are interested in understanding responses to cell death beyond injury, and extending to tissue turnover and homeostasis, as well as developmental cell death and tissue remodeling.
