Research in our laboratory currently spans Immunology, Cell Biology and Neuroscience. We use a variety of approaches including molecular, cell biology, immunology, imaging, genetics and mouse models of development/tissue homeostasis/injury or diseases to address fundamental biological mechanisms. We have a long-term interest in how the immune response is calibrated to avoid chronic inflammation, autoimmunity and self-harm. We study mechanisms that set or limit the magnitude of the immune response. We also study mechanisms that signal the temporal shift from a pathogen-defense mode following successful immune defense to resolution and wound repair. One of the current interests in the lab is cell death and its clearance, and how this can function as a signal for specific effector responses during morphogenesis, homeostatic tissue renewal, or resolution and wound repair after damage. We hypothesize that the integration of cell death recognition, environmental signals (including tissue-specific signals) and the identity of the efferocyte (the cell that recognizes dead cells) determines the specificity for removal of dead/damaged cells, renewal of lost cells, or repair and regeneration.
- Macrophage-stromal interactions during tissue homeostasis and wound repair
- Cell death sensing and innate immune checkpoints in anti-tumor immunity
The brain is commonly acknowledged to be the “last frontier” in human biology. Neurodegenerative disorders including Alzheimer’s Disease and other dementias are currently untreatable and expected to significantly rise in incidence as life expectancy increases. While approaches towards understanding and treating neurological diseases commonly focus on neurons, non-neuronal cells such as glial cell – astrocytes and oligodendrocytes – and microglia exceed the number of neurons in the mammalian nervous system. Glia and immune cells participate in constant bi-directional information exchanges with neurons. We are currently studying these exchanges that play vital roles in maintaining tissue homeostasis and avoid neuroinflammation. We are also studying how disruptions of these neuro-glia-immune communication networks give rise to pathological settings that exacerbate neuronal dysfunction and promote disease progression.
- Astrocytes, oligodendrocytes and microglia during the formation, function and after injury in the nervous systems