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John

John Mountz MD, PhD

Associate Professor of Geriatrics, Department of Medicine, University of Alabama at Birmingham | Professor of Medicine, Division of Clinical Immunology and Rheumatology, Department of Medicine, The University of Alabama at Birmingham

VA Birmingham health care

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Personal Statement

John D. Mountz, MD, PhD, a Birmingham VA Medical Center physician and investigator and Goodwin Blackburn Research Chair in Rheumatology, has been Director of the Birmingham VA Medical Center Comprehensive Flow Cytometry Core since 2008.  Dr. Mountz is a member of the American Society of Clinical Investigation (ASCI) and the Association of American Physicians (AAP) and actively reviews grants for the VA Merit Review, NIH, Alliance for Lupus Research (ALR) and Arthritis Foundation. He received the American College of Rheumatology (ACR) Distinguished Basic Investigator Award in 2016 and the ACR Master Award in 2017. 

Dr. Mountz has an exemplary record in training young investigators, including MD and PhD scientists, in rheumatic disease research.  Dr. Mountz was the first investigator to utilize T cell receptor transgenic mice to address the role of defective T cell tolerance in autoimmunity, to establish a critical role for the lpr gene in regulating peripheral T cell tolerance induction and to propose that defective apoptosis contributed to autoimmunity. He has expertise and experience in answering fundamental and translational questions relevant to rheumatic disease using the techniques of gene targeting, flow cytometry, confocal imaging, super-resolution imaging, and more recently single cell transcriptomes and BCR/TCR sequence analyses.  Dr. Mountz has made several seminal contributions to the field of cell-specific gene therapy for rheumatoid arthritis, the role of B-T cell interactions related to abnormal helper T cell cytokine milieu in the formation of autoreactive germinal centers, and the pathogenic role of type I interferons in shaping autoreactive B cell development in both SLE patients and mouse models of lupus. 


Education

  • BS, Wright State University
  • MS, Michigan State University
  • PhD, Michigan State University
  • MD, Ohio State University

Research Interests

  • Apoptosis Mechanisms of RA and OA Synovial Fibroblasts and Mechanisms Leading to Bone     Erosion
  • Elucidation of the Roles of Fas-mediated Apoptosis in Autoimmune Disease
  • Demonstration of the Roles of Upregulation of Activation-induced Cytidine Deaminase (AID), T-helper 17 cells (Th17) and Interleukin 17 (IL-17), Plasmacytoid Dendritic Cells (pDC), Follicular T helper cells (Tfh), and Marginal Zone Macrophages (MZM) in the Development of Germinal Centers (GCs) Engaged in the Production of Pathogenic IgG Autoantibodies in the Spontaneous Autoimmune BXD2 Model

Recent Publications

  • Hsu H-C, Yang PA, Wu Q, Wang J, Godwin J, Guentert T, Li J, Stockard CR, Le T, Chaplin DD, Grizzle WE, & Mountz, JD.  Inhibition of the catalytic function of activation-induced cytidine deaminase (AICDA) promotes apoptosis of germinal center B cells.  Arthritis Rheum. 2011; 63(7): 2038-2048.  PMCID: PMC3379710.
  • Ding Y, Li J, Wu Q, Yang P, Luo B, Xie S, Druey KM, Zajac AJ, Hsu H-C, & Mountz JD.  IL-17RA       is essential for optimal localization of follicular T helper cells in the germinal center light zone topromote autoantibody-producing B cells.  J Immunol. 2013; 191: 1614-1624.  PMCID: PMC3819396.
  • Li H, Wu Q, Li J, Yang P, Zhu Z, Luo B, Hsu H-C, & Mountz JD. Cutting Edge: Defective follicular exclusion of apoptotic antigens due to marginal zone macrophage defects in autoimmune BXD2 mice.  J Immunol. 2013; 190(9): 4465-4469.  PMCID: PMC3656168.
  • Li J, Hsu HC, Ding Y, Li H, Wu Q, Yang P, Luo B, Rowse AL, Spalding DM, Bridges SL Jr, Mountz JD.  Inhibition of fucosylation reshapes inflammatory macrophages and suppresses type II collagen-induced arthritis. Arthritis Rheumatol. 2014;  66(9): 2368-79. PMCID: PMC4146698
  • Li H, Hsu H-C, Wu Q, Yang PA, Li J, Luo B, Cua D, Oukka M, Steele III CH, Grizzle, WE, & Mountz JD.  IL-23 promotes TCR-mediated negative selection of thymocytes through the upregulation of IL-23 receptor and RORγt.  Nat Commun. 2014; 5: 4259. PMCID: PMC4136447.