Defining the Spatial Localization of Human Innate Cell Precursors in Tissue by IMC | Emily Mace ,PhD

Hear how Emily Mace at Columbia University Irving Medical Center in New York is working to understand the spatial relationship between natural killer (NK) cell precursors and other immune cells and relevant cytoarchitecture using Imaging Mass Cytometry™. Human NK cells are critical immune effector cells that control viral infection and malignancy. Their importance is underscored by the severe disease that occurs when their development is impaired or dysregulated. In the work she describes here, her lab seeks to understand the molecular events that drive NK cell differentiation from common lymphoid progenitors.

ABOUT THIS WEBINAR:

In this webinar presented initially at the CYTO® 2020 virtual meeting, Mace introduces her lab’s approach to answer key questions about human NK cell development. She discusses:

- The spectrum of developmental intermediates that show increasingly restricted lineage potential that can be isolated from tissue and give rise to mature, functional NK cells
- The spatial localization of NK cell developmental intermediates within human secondary lymphoid tissue
- Preliminary findings that provide an exciting foundation for the first in situ roadmap of human innate immune cell development in tissue

ABOUT THE PRESENTER:

Emily Mace, PhD
Assistant Professor of Pediatric Immunology
Columbia University Irving Medical Center

Emily Mace studies human natural killer cell development, particularly with quantitative image analysis and cell biological approaches. This includes the use of highly spatially and temporally resolved and super-resolution microscopy to understand interactions between NK cell precursors and the microenvironment. She also identifies novel requirements for human NK cell development through the identification and study of rare patients with NK cell deficiencies. This has included the characterization of NK cell functional and cell biological phenotypes associated with MCM10, GATA2, IRF8 and coronin 1A deficiencies.