Professor, Department of Pathology
Samuel A. Brown Professor of Medicine, Department of Medicine
Major areas of research in my lab include stem cells in normal hematopoiesis and leukemia, dendritic cell development and function, and mechanisms of autoimmunity.
Stem Cells in Normal Hematopoiesis and Leukemia
Stem cells can both differentiate into various cell types and maintain their own population of undifferentiated cells. Thus, a single hematopoietic stem cell (HSC) can regenerate the entire blood system in irradiated recipients, enabling a potentially life-saving bone marrow transplantation. However, controversies remain on the role and properties of HSCs during normal blood production—hematopoiesis—in unirradiated organisms.
We have developed genetic tools to identify and trace HSCs, and we have shown that these cells are indeed a major source of adult hematopoiesis. Our current studies focus on the mechanisms of HSC differentiation in normal conditions and their subversion in leukemia.
Dendritic Cell Development and Function
Dendritic cells (DCs) detect, capture, and present invading pathogens to lymphocytes, thus representing a critical link between innate and adaptive immunity. DCs encompass several lineages dedicated to distinct pathogens and immune response types, including the antigen-presenting classical DCs (cDCs) and interferon-producing plasmacytoid DCs (pDCs).
Our studies have identified several transcription factors and signaling pathways that control the development and specification of DCs. Our current studies focus on the molecular control of DC function in the steady state and during immune responses.
Mechanisms of Autoimmunity
Aberrant recognition and attack of the body by its own immune system causes autoimmune diseases such as type 1 diabetes, multiple sclerosis, and systemic lupus erythematosus (SLE). We are studying the mechanisms of autoimmunity by focusing on SLE, in which the immune system targets self-DNA and self-RNA. We have characterized a unique nuclease, DNASE1L3, as an essential mechanism of tolerance to self-DNA, the loss of which causes SLE-like autoimmune responses towards self-DNA. We are exploring the mechanism of DNASE1L3 activity and its potential as a therapeutic tool.
Samuel A. Brown Professor of Medicine, Department of Medicine at NYU Grossman School of Medicine
Co-Director, Judith and Stewart Colton Center for Autoimmunity
Director, Translational Immunology Center
Nature immunology. 2023 Jan; 24(1):84-95
Immunity. 2022 Mar 08; 55(3):405-422.e11
Journal of experimental medicine. 2021 May 03; 218(5):
Science immunology. 2021 Apr 02; 6(58):
American journal of human genetics. 2020 Nov 05; 107(5):882-894
Annual review of cell & developmental biology. 2020 Oct 06; 36:529-550
Cell stem cell. 2020 Aug 06; 27(2):336-345.e4
Immunity. 2020 Jun 16; 52(6):1022-1038.e7