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

  • EDELSONB@WUSTL.EDU

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

  • Immune cell development and function

Research Abstract:

My laboratory is focused on two areas of immunology. First, we are interested in understanding how autoreactive T cells mediate autoimmune disease, particularly in multiple sclerosis (MS) and its mouse model, experimental autoimmune encephalomyelitis (EAE). We focus on how cytokine expression is regulated in autoreactive T cells in a cell-intrinsic manner through the action of transcription factors, and how these cytokines mediate disease pathogenesis. We are particularly interested in how T cell expression of granulocyte-macrophage colony stimulating factor (GM-CSF) and interleukin-10 (IL-10) is regulated, and how these cytokines act on cells of the innate immune system during autoimmune disease. My laboratory`s work in this area led to our discovery that the transcription factor Bhlhe40 regulates cytokine production by CD4+ T cells. Second, we are interested in understanding the development, heterogeneity, and function of monocytes, macrophages, and dendritic cells during immune responses. We use a variety of gene-deficient mice to analyze how specific monocyte, macrophage, and dendritic cell subsets carry out their non-redundant roles during autoimmunity and infection. We employ mouse models of Listeria monocytogenes and Heligmosomoides polygyrus infections in many of these experiments.

Selected Publications:

Huynh JP, Lin CC, Kimmey JM, Jarjour NN, Schwarzkopf EA, Bradstreet TR, Shchukina I, Shpynov O, Weaver CT, Taneja R, Artyomov MN, Edelson BT*, Stallings CL*. Bhlhe40 is an essential repressor of IL-10 during Mycobacterium tuberculosis infection. J Exp Med. 2018 Jul 2;215(7):1823-1838. *Co-corresponding authors.

Lin CC, Edelson BT. New Insights into the Role of IL-1β in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis. J Immunol. 2017 Jun 15;198(12):4553-4560.

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.

Last Updated: 7/27/2018 11:29:55 AM

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