JoAnne L. Flynn, PhD
Professor
W1144 Biomedical Science Tower
200 Lothrop Street
Education
PhD in Microbial Genetics/Pathogenic Mechanisms, University of California, Berkeley
Research Summary
My primary interest is in the interaction of pathogens with the host, with special emphasis on the immune mechanisms that protect against or exacerbate disease. Our focus is on Mycobacterium tuberculosis, the organism responsible for tuberculosis, which causes 2 million deaths per year worldwide. We are investigating the immune responses required for protection against tuberculosis, and the effect of these immune responses on both the host and the bacterium. We specifically study cytokine production, macrophage activation, and T cell subsets (CD4+ and CD8+ T cells) that are important in tuberculosis. Finally, we have a strong interest in the immune mechanisms responsible for maintaining a latent M. tuberculosis infection, and how deficiencies in the immune response can result in reactivation of disease. Our work is done in two model systems: mice and non-human primates. We have vaccine studies, drugs studies, and basic immunologic and pathogenesis studies ongoing. We also participate in projects involving mathematical modeling of the immune response to M. tuberculosis, and our plan is to incorporate nuclear imaging of live animals into our research.
Research Lab Affiliation
Publications
HIV-1/mycobaterium tuberculosis co-infection immunology: How does HIV exacerbate TB? Infect Immun. 79: 1407-1417. | View Abstract
Tuberculosis: What we don’t know can, and does, hurt us. Science. 328: 852-856. | View Abstract
TNF and IL-10 are major factors in modulation of the phagocytic cell environment in lung and lymph node in tuberculosis: a next generation two compartmental model. J Theoretical Biology. 265: 586-598. | View Abstract
CD4(+) Regulatory T cells in a Cynomolgus Macaque Model of Mycobacterium tuberculosis Infection. J Infect Dis. 202: 533-541. | View Abstract
Reactivation of latent tuberculosis in cynomolgus macaques infected with SIV is associated with early peripheral T cell depletion and not virus load. PloS One. 5: e9611. | View Abstract
Infection with Helicobacter pylori is associated with protection against tuberculosis. PLoS One. 5: e8804. | View Abstract
Tumor necrosis factor neutralization results in disseminated disease in acute and latent Mycobacterium tuberculosis infection with normal granuloma structure in a cynomolgus macaque model. Arthritis Rheum. 62: 340-350. | View Abstract

