JoAnne L. Flynn, PhD

Professor


Dr. Flynn

Contact

412-624-7743
Fax: 412-648-3394

W1144 Biomedical Science Tower

200 Lothrop Street

Pittsburgh, PA 15261-2111

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