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
Director, Translational Immunology Center
PhD from Weizmann Institute of Science
Journal of immunology (Baltimore, Md. : 1950). 2023 Nov 15; 211(10):1475-1480
Blood. 2023 Aug 03; 142(5):460-476
Nature immunology. 2023 Aug; 24(8):1265-1280
Journal of experimental medicine. 2023 Jun 05; 220(6):
Proceedings of the National Academy of Sciences of the United States of America (PNAS). 2023 May 30; 120(22):e2302019120
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):