Dr. Reizis joined UChicago in 2025 from the NYU Grossman School of Medicine, where he has been the Samuel A. Brown Professor of Medicine and a founding director of the Translational Immunology Center. His lab is studying fundamental mechanisms of immune system development, immunological tolerance and autoimmunity.
One major area of research is dendritic cells (DCs), innate sentinel cells that comprise the antigen-presenting classical DCs (cDCs) and interferon-producing plasmacytoid DC (pDCs). The Reizis lab has identified several key transcriptional regulators and signaling pathways that control the DC lineage, such as the "master regulator" of pDC development (TCF4/E2-2), the driver of cDC differentiation in the periphery (NOTCH2) and the common regulator of pDC and cDC development (TRIM33). Recent studies have characterized the role of 3D chromatin organization in the differentiation and/or function of cDCs and pDCs. Finally, the lab has identified transcription factor ETV3 as a specific regulator of cDC maturation that enables the tolerogenic function of DC in the steady state. These genetic insights are used to better characterize the role of DCs in immune response to infections, immune homeostasis and autoimmunity.
The lab also studies systemic autoimmune diseases such as systemic lupus erythematosus (SLE), which is characterized by autoreactivity to nuclear antigens including ribonucleoproteins and DNA. Of particular interest are antibody responses to self DNA, which are prevalent and pathogenic in SLE. The lab has defined the extracellular nuclease DNASE1L3 as an essential gatekeeper of tolerance to self-DNA, and revealed its autoantibody-mediated blockade in more than half of human patients with severe SLE. Current studies include the mechanisms that cause the breakdown of tolerance and propagation of autoreactivity in SLE and its animal models.
Transcription factor Etv3 controls the tolerogenic function of dendritic cells.
Transcription factor Etv3 controls the tolerogenic function of dendritic cells. Science. 2026 Feb 12; 391(6786):eads1246.
PMID: 41678619
Chromatin-mediated anticipatory control of type I interferon production in plasmacytoid dendritic cells.
Chromatin-mediated anticipatory control of type I interferon production in plasmacytoid dendritic cells. Immunity. 2026 Feb 10; 59(2):270-287.e11.
PMID: 41672043
Cohesin-mediated chromatin organization controls the differentiation and function of dendritic cells.
Cohesin-mediated chromatin organization controls the differentiation and function of dendritic cells. Sci Immunol. 2026 Feb 06; 11(116):eadx4622.
PMID: 41650249
Early-onset systemic lupus erythematosus-ANCA-associated vasculitis overlap syndrome caused by DNASE1L3 deficiency.
Early-onset systemic lupus erythematosus-ANCA-associated vasculitis overlap syndrome caused by DNASE1L3 deficiency. Rheumatology (Oxford). 2025 Dec 01; 64(12):6432-6434.
PMID: 40880305
Tonic type I interferon signaling optimizes the antiviral function of plasmacytoid dendritic cells.
Tonic type I interferon signaling optimizes the antiviral function of plasmacytoid dendritic cells. Nat Immunol. 2025 Nov; 26(11):1946-1961.
PMID: 41087726
Peritumoral macrophages recruit eosinophils to promote antitumor immune responses in breast cancer.
Peritumoral macrophages recruit eosinophils to promote antitumor immune responses in breast cancer. Proc Natl Acad Sci U S A. 2025 Sep 23; 122(38):e2504645122.
PMID: 40953260
Dynamic remodeling of the pancreas immune landscape in obesity.
Dynamic remodeling of the pancreas immune landscape in obesity. Res Sq. 2025 Aug 27.
PMID: 40909804
Dynamic remodeling of the pancreas immune landscape in obesity.
Dynamic remodeling of the pancreas immune landscape in obesity. bioRxiv. 2025 Jul 18.
PMID: 40791478
Spatial and single cell mapping of castleman disease reveals key stromal cell types and cytokine pathways.
Spatial and single cell mapping of castleman disease reveals key stromal cell types and cytokine pathways. Nat Commun. 2025 Jul 01; 16(1):6009.
PMID: 40593805
Plasma DNA Profile Associated with DNASE1L3 Gene Mutations: Clinical Observations, Relationships to Nuclease Substrate Preference, and In Vivo Correction.
Plasma DNA Profile Associated with DNASE1L3 Gene Mutations: Clinical Observations, Relationships to Nuclease Substrate Preference, and In Vivo Correction. Am J Hum Genet. 2025 May 01; 112(5):1247.
PMID: 40315821