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Faculty Detail    
Name FRANCES E. LUND
Charles H. McCauley Professor and Chair of the Department of Microbiology
 
Campus Address BBRB 276 Zip 2170
Phone 205-934-9339
E-mail flund@uab.edu
Other websites The Lund & Randall Labs
Publications
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Microbiology  Microbiology Professor
Secondary  Medicine  Med - Immunology/Rheumatology Professor
Center  Arthritis & Musculoskeletal Diseases Center  Arthritis & Musculoskeletal Diseases Center Professor
Center  Center for AIDS Research  Center for AIDS Research Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Professor

Biographical Sketch 
Frances (Fran) Lund completed her undergraduate studies in Microbiology at the University of Notre Dame (B.S., cum laude, 1987). She performed her graduate work with Dr. Ronald B. Corley in the Department of Microbiology at Duke University. She obtained her Ph.D. in Immunology in 1992 and went on to a post-doctoral immunology fellowship in Dr. Maureen Howard’s group at DNAX Research Institute in Palo Alto, CA. In 1997 she moved to the Trudeau Institute, a basic biomedical infectious disease research institute, and started her own research lab. Over the next 11 years, Dr. Lund and her scientific partner, Dr. Troy Randall, developed research programs studying humoral and cellular immune responses to pulmonary and intestinal pathogens. In 2008, they joined the University of Rochester as Professors within the Division of Allergy, Immunology and Rheumatology (Department of Medicine). Over the next four years, Dr. Lund developed additional research programs in autoimmunity and allergy and began her work in human translational immunology. In 2012, Drs. Lund and Randall and their joint labs were recruited to UAB. Dr. Lund is currently serving as the Charles H. McCauley Professor and Chair of the Department of Microbiology. She holds a secondary appointment in the Division of Clinical Immunology and Rheumatology and is a senior scientist in the Comprehensive Cancer Center and the Comprehensive Arthritis, Musculoskeletal and Autoimmunity Center.

Research/Clinical Interest
Title
B lymphocytes in infection, allergy and autoimmune disease. Regulation of inflammation, oxidative stress and metabolic fitness
Description
The overarching research objective of the Lund laboratory is to identify the key players that suppress or exacerbate mucosal inflammatory responses with the long-term goal of developing therapeutics to treat immunopathology associated with chronic infectious, allergic and autoimmune disease. To evaluate inflammation and cellular immune responses in vivo, we utilize different strains of mice that have genetically altered immune systems. We expose these mice to pathogens, allergens or autoantigens and then study the ensuing inflammatory immune response in lymphoid organs and in mucosal tissues like the lung and gut. We study inflammatory responses in mice that spontaneously develop autoimmune diseases like Systemic Lupus Erythematosus (SLE), Rheumatoid Arthritis (RA) or Type 1 Diabetes (T1D). We also examine inflammatory responses in mice exposed to common allergens like house dust mite or infected with viral, bacterial, fungal or parasitic pathogens. Finally, we expose mice to toxins like cigarette smoke and DNA-damaging chemotherapeutics and monitor chronic inflammation and tissue damage in sites such as the lung. In one project, we are characterizing the roles that cytokine-producing “effector” B cells play in modulating inflammation and T cell-mediated immune responses to pathogens, autoantigens and allergens. Using transcriptome and proteome analysis, we have defined cytokine-producing effector B cell “signatures” in both laboratory mice and humans and are now addressing whether any of these newly identified effector B cell subsets are inappropriately expanded or missing in autoimmune patients. In addition, we are using mouse autoimmune models to determine whether depletion of specific effector B cell subsets alters humoral and cellular immunity and attenuates disease-mediated pathology. If so, then biologics that target these “pathogenic” effector B cell subsets may represent novel and more specific targets for the treatment of diseases like RA, SLE and T1D. Similarly, we are addressing how cytokine-producing and antigen-presenting B cells regulate allergic disease. Recent studies from the lab demonstrated that we can significantly attenuate allergic responses in animals using biologics that transiently deplete B cells, or block particular cytokines made by these B cells, or block the downstream target of the B cell-derived cytokines. The focus of the current studies is to determine at a molecular level how these cytokine-producing B cells are induced and whether we can prevent their amplification or maintenance in animals that have already developed allergic disease. In addition, we are actively evaluating how the cytokine-producing B cells initiate the allergic disease process and regulate the function of the dendritic cells and CD4 T cells which cause disease. Another project in my laboratory uses the influenza infection model to evaluate how B cells and the antibodies made by B cells contribute to local pulmonary protection from reinfections with the virus. We know that memory B cells and the antibodies made by long-lived plasma cells play critical roles in immune protection from challenge infections with influenza virus, yet we know very little about the factors that control the generation, maintenance and survival of memory B cells or plasma cells, particularly within the lung microenvironment. One of our goals is to identify the protective niches within the lung and lymphoid tissues that can sustain the long-term survival of plasma cells and memory B cells and to determine how these niches are regulated both developmentally and in response to inflammatory signals. A second goal is to identify the inflammatory signals that regulate the balance between the development of the antibody-producing long-lived plasma cells and the memory B cell compartment. Finally, my lab studies how oxidative stress induced by reactive oxygen species (ROS) impacts inflammation, immune responses and cellular metabolism. Specifically, we address how the NAD-consuming enzymes, CD38 and PARP1, and the TRPM2 cation channel (activated by NAD and NAD-derived catabolites) regulate the redox balance in immune cells and affect the activity, function and survival of these cells following exposure to toxins such as cigarette smoke or chemotherapeutics like DNA alkylating drugs. Our current experiments are directed at determining how CD38 and TRPM2 enhance the ability of immune cells and tumor cells to withstand the damage associated with inflammation-induced ROS and whether, by manipulating the NAD metabolome, we can alter the survival or function of these potentially pathogenic cells.

Selected Publications 
Publication PUBMEDID
Selected publications from 2011-to present. For complete list see NCBI URL Link in FACULTY DETAIL at the top of this page  99999999 
Etich J, Bergmeier V, Frie C, Kreft S, Bengestrate L, Eming S, Mauch C, Eckes B, Ulus H, Lund FE, Rappl G, Abken H, Paulsson M, Brachvogel B. PECAM1(+)/Sca1(+)/CD38(+) Vascular Cells Transform into Myofibroblast-Like
Cells in Skin Wound Repair. PLoS One. 2013;8(1):e53262.  
23308177 
Oleksyn D, Pulvino M, Zhao J, Misra R, Vosoughi A, Jenks S, Tipton C, Lund F, Schwartz G, Goldman B, Mohan C, Mehta K, Mehta M, Leitgets M, Sanz I, Chen L. PKCbeta is required for lupus development in Sle mice. Arthritis Rheum. 2012   23280626 
Levy A, Blacher E, Vaknine H, Lund FE, Stein R, Mayo L. CD38 deficiency in the tumor microenvironment attenuates glioma progression and modulates features of tumor-associated microglia/macrophages. Neuro Oncol. 2012 Aug;14(8):1037-49.   22700727 
León B, Ballesteros-Tato A, Browning JL, Dunn R, Randall TD, Lund FE. Regulation of T(H)2 development by CXCR5+ dendritic cells and lymphotoxin-expressing B cells. Nat Immunol. 2012 May 27;13(7):681-90.   22634865 
Ballesteros-Tato A, León B, Graf BA, Moquin A, Adams PS, Lund FE, Randall TD. Interleukin-2 inhibits germinal center formation by limiting T follicular helper cell differentiation.Immunity. 2012 May 25;36(5):847-56.   22464171 
León B, Ballesteros-Tato A, Misra RS, Wojciechowski W, Lund FE. Unraveling effector functions of B cells during infection: the hidden world beyond antibody production. Infect Disord Drug Targets. 2012 Jun;12(3):213-21.   22394173 
du Pré MF, van Berkel LA, Ráki M, van Leeuwen MA, de Ruiter LF, Broere F, Ter Borg MN, Lund FE, Escher JC, Lundin KE, Sollid LM, Kraal G, Nieuwenhuis EE, Samsom JN. CD62L(neg)CD38+ expression on circulating CD4+ T cells identifies mucosally differentiated cells in protein fed mice and in human celiac disease patients and controls. Am J Gastroenterol. 2011 Jun;106(6):1147-59.   21386831 
Lamere MW, Moquin A, Lee FE, Misra RS, Blair PJ, Haynes L, Randall TD, Lund FE, Kaminski DA. Regulation of antinucleoprotein IgG by systemic vaccination and its effect on influenza virus clearance. J Virol. 2011 May;85(10):5027-35.   21367900 
LaMere MW, Lam HT, Moquin A, Haynes L, Lund FE, Randall TD, Kaminski DA. Contributions of anti-nucleoprotein IgG to heterosubtypic immunity against influenza virus. J. Immunol. 2011 186:4331-4339.   21357542 

Keywords
Immunology, infectious disease, autoimmunity, cancer