Duke University Medical Center
research The Garcia-Blanco Lab

Brandt Levitt
Graduate Student

Brandt Levitt 2005 - University of Wisconsin
BS, Bacteriology

2007-2009 University of Colorado
Academic Research

2009 - Present - Duke University
Graduate Student: Molecular Genetics and Microbiology Program

  Phone: 919.613.8633
Email: brandt.levitt@duke.edu


Brandt Levitt began his academic career at the University of Wisconsin – Madison in the Bacteriology department. While studying microbial physiology, host pathogen interactions and innate immunity, he worked in the laboratory of Patricia Keely of the pharmacology department, where he dissected the role of the R-Ras oncogene in aberrant cellular signaling that results in breast cancer. After his bachelors degree, Brandt spent three years in the biotechnology industry, developing molecular diagnostics tests for infectious diseases ranging from RNA viruses to drug resistant bacteria for Third Wave Technologies. Brandt then went on to study the innate immune system and autoimmunity in the laboratory of Michael Holers at the University of Colorado, publishing half a dozen articles about complement and Rheumatoid Arthritis. In 2009, Brandt joined the Duke Molecular Genetics and Microbiology Phd program because of its strength in host-pathogen interactions. In 2010, he joined the Garcia-Blanco laboratory where he studies exonucleases that act as pro-flaviviral host factors for Dengue and Yellow Fever Virus RNA replication. He anticipates a career in public health, utilizing the problem solving and critical thinking skills gained through research.


1) Initiation of the Alternative Pathway of Murine Complement by Immune Complexes is Dependent on N-Glycans in IgG Antibodies. Banda NK, Takahashi M, Wood A, Levitt B, Rudd P, Royle L, Abrahams J, Stahl G, Holers VM, Arend WP. Arthritis and Rheumatism Vol 58 No. 10, October 2008 pp 3081-3089

2) Targeted Inhibition of the Complement Alternative Pathway with Complement Receptor 2 and Factor H Attenuates Collagen Antibody-Induced Arthritis in Mice. Banda NK, Levitt B, Glogowska MJ, Thurman JM, Takahashi K, Stahl GL, Tomlinson S, Arend WP, and Holers VM. J. Immunol., Nov 2009; 183: 5928 - 5937.

3) Complement activation pathways in murine immune complex-induced arthritis and in C3a and C5a generation in vitro. Banda, NK, Levitt, B, Wood, AK, Takahashi K, Stahl GL, Holers VM and Arend WP. Clinical & Experimental Immunology, 159: 100108. 1365-2249. October 2009.

4) Treatment with Cl-amidine, a peptidyl arginine deiminase (PAD) inhibitor, significantly reduces collagen-induced arthritis (CIA). Willis VC, Gizinski A, Banda NK, Knuckley B, Cordova K, Causey CP, Levitt B, Glogowska MJ, Benbarak M, Chandra P, Kulik L, Arend WP, Robinson WH, Thompson PR, and Holers VM. J. Immunol., Apr 2009; 182: 50.6.

5) Essential Role of Complement Mannose-Binding Lectin-Associated Serine Proteases-1/3 in the Murine Collagen Antibody-Induced Model of Inflammatory Arthritis. Banda NK, Levitt B, Takahashi M, Glogowska M, Nicholas J, Takahashi K, Stahl GL, Fujita T, Arend WP, Holers VM. J Immunol. 2010 Sep 24