Faculty

Boris Reizis, PhD

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.

Dynamic remodeling of the pancreas immune landscape in obesity.
Dynamic remodeling of the pancreas immune landscape in obesity. Nat Commun. 2026 07 28; 17(1).
PMID: 42660905

Dendritic Cell Heterogeneity Tailored to Their Function.
Dendritic Cell Heterogeneity Tailored to Their Function. Immunol Rev. 2026 May; 339(1):e70123.
PMID: 41972485

A Human Lymph node-on-a-Chip for Personalized Evaluation of Vaccine Immunogenicity.
A Human Lymph node-on-a-Chip for Personalized Evaluation of Vaccine Immunogenicity. Res Sq. 2026 Mar 30.
PMID: 41960315

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

DNA origami vaccines program antigen-focused germinal centers.
DNA origami vaccines program antigen-focused germinal centers. Science. 2026 Feb 05; 391(6785):eadx6291.
PMID: 41643005

IFN?-dependent metabolic reprogramming restrains an immature, pro-metastatic lymphatic state in melanoma.
IFN?-dependent metabolic reprogramming restrains an immature, pro-metastatic lymphatic state in melanoma. Cancer Cell. 2026 Apr 13; 44(4):792-808.e9.
PMID: 41576931

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. 2026 Jan 08; 113(1):234.
PMID: 41386233

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

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