ORCID

http://orcid.org/0000-0002-2617-7571

Date of Award

Spring 5-15-2020

Author's School

Graduate School of Arts and Sciences

Author's Department

Biology & Biomedical Sciences (Immunology)

Degree Name

Doctor of Philosophy (PhD)

Degree Type

Dissertation

Abstract

Natural killer cells and Type I innate lymphoid cells (ILCs) are subsets of ILCs. In C57BL/6 mice, they share expression of the surface markers NK1. 1 and NKp46, and can produce the cytokine interferon-gamma. These similarities led to the initial classification of natural killer cells and Type I ILCs together under the category of Group 1 ILCs. However, more recent studies found that natural killer cells and ILC1s develop from distinct progenitor cells and utilize transcription factor in distinct manners. Whereas ILC1s require Tbet for their development and are Eomes-independent, natural killer cells require Tbet only for terminal maturation and are Eomes-dependent. As such, these populations were reclassified as separate ILC subsets. In the context of Toxoplasma gondii infection, we identified a new population that blurs these strict delineations. Our data suggest that T. gondii induces the development of ILC1-like cells that primarily result from the downregulation of Eomes and the upregulation of Tbet. We further validated these findings with epigenomic profiling and single-cell RNA sequencing.

Language

English (en)

Chair and Committee

Wayne M. Yokoyama

Committee Members

Marina Cella, Marco Colonna, Megan Cooper, Gwendolyn Randolph,

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