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Brian Edelson, MD, PhD

Brian Edelson, MD, PhD

Assistant Professor, Pathology & Immunology

Phone314-362-4427

Emailbedelson@wustl.edu

Clinical Interests

  • Immunology

Research Interests

My laboratory is focused on two areas of immunology. First, we are interested in understanding macrophage and dendritic cell (DC) development and heterogeneity. Second, we are interested in understanding the basis for the innate immune response to bacterial infections, using the intracellular bacterium Listeria monocytogenes in a mouse model.

Macrophages and DCs derive from a common hematopoietic progenitor and exist as multiple distinct subtypes in different anatomic microenvironments. In addition, inflammatory states induce the differentiation of unique forms of inflammatory macrophages and DCs from blood-circulating monocyte precursors. We are particularly interested in 1) identifying and characterizing the environmental signals and transcription factors controlling the development and function of macrophage and DC subtypes, and 2) understanding the specific roles played by distinct macrophage and DC subtypes during different immune responses. An understanding of these processes is relevant to pathogen defense, vaccine design, autoimmunity, and tumor immunity, as macrophages and DCs are recognized to play a role in each of these settings. We use comparative gene expression profiling of developing and mature murine macrophage and DC subtypes to identify genes with unique expression patterns potentially important in controlling macrophage and DC development and function. Using genetic approaches, and in particular through the analysis of gene-deficient mice, we aim to identify distinct pathways of macrophage and DC subtype development. Furthermore, we aim to characterize the unique functions of distinct subtypes in vivo.

My laboratory also aims to understand the basis for the innate immune response to bacterial infections, using the intracellular bacterium Listeria monocytogenes in a mouse model. Our goals are to understand the development and interplay of innate immune cells controlling early intracellular infection, and to understand how these cells serve as the basis for the generation of a complete adaptive immune response to a pathogen. Important questions that we aim to address are as follows: 1) Which are the earliest phagocytes infected during intracellular bacterial infection, and how do these cells propagate a productive infection? 2) What are the pathways leading to the development of inflammatory DCs (iDCs) during pathogen infection, and what are their effector roles? 3) How do neutrophils, macrophages, and DCs differ in their handling of intracellular bacteria, and how do these cells carry out microbicidal function?

DBBS Graduate Program Affiliation

  • Immunology
  • Molecular Microbiology and Microbial Pathogenesis

Publications

Pub Med Search

Igyártó BZ, Haley K, Ortner D, Bobr A, Gerami-Nejad M, Edelson BT, Zurawski SM, Malissen B, Zurawski G, Berman J, Kaplan DH. Skin-resident murine dendritic cell subsets promotes distinct and opposing antigen-specific T helper cell responses. Immunity 35:260-272, 2011 Abstract
Edelson BT, Bradstreet TR, Hildner K, Carrero JA, Frederick KE, Kc W, Belizaire R, Aoshi T, Schreiber RD, Miller MJ, Murphy TL, Unanue ER, Murphy KM. CD8a(+) dendritic cells are an obligate cellular entry point for productive infection by Listeria monocytogenes. Immunity 35:236-248, 2011 Abstract
Edelson BT, Bradstreet TR, KC W, Hildner K, Herzog JW, Sim J, Russell JH, Murphy TL, Unanue ER, Murphy KM. Batf3-dependent CD11b peripheral dendritic cells are GM-CSF-independent and are not required for Th cell priming after subcutaneous immunization. PLoS 6(10):e25660, 2011Abstract
Albring JC, Sandau MM, Rapaport AS, Edelson BT, Satpathy A, Mashayekhi M, Lathrop SK, Hsieh CS, Stelljes M, Colonna M, Murphy TL, Murphy KM. Targeting of B and T lymphocyte associated (BTLA) prevents graft-versus-host disease without global immunosuppression. J. Exp. Med. 207: 2551-2559, 2010 Abstract
Bar-On L, Birnberg T, Lewis KL, Edelson BT, Bruder D, Hildner K, Buer J, Murphy KM, Reizis B, Jung S. CX3CR1+ CD8alpha+ dendritic cells are a steady-state population related to plasmacytoid dendritic cells. roc. Natl. Acad. USA 107: 14745-14750, 2010 Abstract
Edelson BT, KC W, Juang R, Kohyama M, Benoit LA, Klekotka PA, Moon C, Albring JC, Ise W, Michael DG, Bhattacharya D, Stappenbeck TS, Holtzman MJ, Sung SJ, Murphy TL, Hildner K, Murphy KM. Peripheral CD103+ dendritic cells form a unified subset developmentally related to CD8a+ conventional dendritic cells. J. Exp. Med. 207: 823-836, 2010 Abstract
Kohyama M, Ise W, Edelson BT, Wilker PR, Hildner K, Mejia C, Frazier WA, Murphy TL, Murphy KM. Role for Spi-C in the development of red pulp macrophages and splenic iron homeostasis. Nature 457: 318-321, 2009 Abstract
Hildner K, Edelson BT, Purtha WE, Diamond M, Matsushita H, Kohyama M, Calderon B, Schraml BU, Unanue ER, Diamond MS, Schreiber RD, Murphy TL, Murphy KM.. Batf3 deficiency reveals a critical role for CD8alpha+ dendritic cells in cytotoxic T cell immunity.. Science 322: 1097-1100., 2008 Abstract


Lab Phone: 314-362-4428