Brian T. Edelson, M.D., Ph.D.

Assistant Professor
Pathology and Immunology
Laboratory and Genomic Medicine

Immunology Program
Molecular Microbiology and Microbial Pathogenesis Program

  • 314-362-4427

  • 314-362-4428

  • 314-747-7903

  • 8118

  • Room 8413 BJCIH


  • dendritic cells, macrophaes, hematopoiesis, infection, inflammation, innate immunity, autoimmunity, multiple sclerosis

  • Immune cell development and function

Research Abstract:

My laboratory is focused on three areas of immunology. First, we aim to understand how the cytokine GM-CSF contributes to autoimmunity, particularly using a mouse model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE). Second, we are interested in understanding macrophage and dendritic cell (DC) development and heterogeneity. Third, 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.

1) GM-CSF is a pleiotropic cytokine produced by many immune and non-immune cells. In EAE it is produced by autoreactive T cells, and plays a non-redundant role. We are aimed at understanding the transcriptional basis for GM-CSF production by T cells, and discerning how inflammatory immune cells respond to this cytokine.

2) 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.

3) 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?

Selected Publications:

Lin CC, Bradstreet TR, Schwarzkopf EA, Jarjour NN, Chou C, Archambault AS, Sim J, Zinselmeyer BH, Carrero JA, Wu GF, Taneja R, Artyomov MN, Russell JH, Edelson BT. IL-1-induced Bhlhe40 identifies pathogenic T helper cells in a model of autoimmune neuroinflammation. J. Exp. Med. 2016 213: 251-271.

Lin C-C, Bradstreet TR, Schwarzkopf EA, Sim J, Carrero JA, Chou C, Cook LE, Egawa T, Taneja R, Murphy TL, Russell JH, Edelson BT. Bhlhe40 controls cytokine production by T cells and is essential for pathogenicity in autoimmune neuroinflammation. Nat. Commun. 2014 5: 3551.

Edelson BT. Dendritic cells in Listeria infection. Adv Immunol 2012 113:33-49.

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 One 2011 6(10): e25660.

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 2011 35: 326-48.

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. 2010 207: 823-836.

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 2009 457: 318-321.

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 2008 322: 1097-1100.

Last Updated: 9/1/2016 9:24:52 AM

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