Division of Rheumatology, Department of Medicine, Washington University School of Medicine, St. Louis, United States
Swapneel Patel
Division of Rheumatology, Department of Medicine, Washington University School of Medicine, St. Louis, United States
Qiuling Wang
Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, United States
Prabhakar Andhey
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, United States
Konstantin Zaitsev
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, United States; Computer Technologies Department, ITMO University, Saint Petersburg, Russia
Sophia Porter
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, United States
Maxwell Hershey
Division of Rheumatology, Department of Medicine, Washington University School of Medicine, St. Louis, United States
Michael Bern
Division of Rheumatology, Department of Medicine, Washington University School of Medicine, St. Louis, United States
Beatrice Plougastel-Douglas
Division of Rheumatology, Department of Medicine, Washington University School of Medicine, St. Louis, United States
Patrick Collins
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, United States
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, United States
Kenneth M Murphy
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, United States
Eugene Oltz
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, United States; Department of Microbial Infection and Immunity, Ohio State University Wexner School of Medicine, Columbus, United States
Maxim Artyomov
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, United States
L David Sibley
Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, United States
Innate lymphoid cells (ILCs) were originally classified based on their cytokine profiles, placing natural killer (NK) cells and ILC1s together, but recent studies support their separation into different lineages at steady-state. However, tumors may induce NK cell conversion into ILC1-like cells that are limited to the tumor microenvironment and whether this conversion occurs beyond this environment remains unknown. Here, we describe Toxoplasma gondii infection converts NK cells into ILC1-like cells that are distinct from both steady-state NK cells and ILC1s in uninfected mice. These cells were Eomes-dependent, indicating that NK cells can give rise to Eomes– Tbet-dependent ILC1-like cells that circulate widely and persist independent of ongoing infection. Moreover, these changes appear permanent, as supported by epigenetic analyses. Thus, these studies markedly expand current concepts of NK cells, ILCs, and their potential conversion.
