JoAnne L. Flynn, PhD


Dr. Flynn


Fax: 412-648-3394

5058 Biomedical Science Tower 3

3501 Fifth Avenue

Pittsburgh, PA 15260


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


Myers, A. M; Marino, S; Kirschner, D. E and Flynn, J. L. Inoculation dose of Mycobacterium tuberculosis does not influence priming of T cell responses in lymph nodes. J. Immunol. [In press] 2013. |  

Green, A. M; Difazio, R and Flynn, J. L. IFN-gamma from CD4 T cells is essential for host survival and enhances CD8 T cell function during Mycobacterium tuberculosis infection. J Immunol. 190: 270-277. |  View Abstract

Via, L. E; Schimel, D; Weiner, D. M; Dartois, V; Dayao, E; Cai, Y; Yoon, Y. S; Dreher, M. R; Kastenmayer, R. J; Laymon, C. M; Carny, J. E; Flynn, J. L; Herscovitch, P and Barry, C. E., 3rd. Infection dynamics and response to chemotherapy in a rabbit model of tuberculosis using [(1)(8)F]2-fluoro-deoxy-D-glucose positron emission tomography and computed tomography. Antimicrob Agents Chemother. 56: 4391-4402. |  View Abstract

Phuah, J. Y; Mattila, J. T; Lin, P. L and Flynn, J. L. Activated B cells in the granulomas of nonhuman primates infected with Mycobacterium tuberculosis. Am J Pathol. 181: 508-514. |  View Abstract

Lin, P. L; Rutledge, T; Green, A. M; Bigbee, M; Fuhrman, C; Klein, E and Flynn, J. L. CD4 T Cell Depletion Exacerbates Acute Mycobacterium tuberculosis While Reactivation of Latent Infection Is Dependent on Severity of Tissue Depletion in Cynomolgus Macaques. AIDS Res Hum Retroviruses. [Epub ahead of print] |  View Abstract

Lin, P. L; Dartois, V; Johnston, P. J; Janssen, C; Via, L; Goodwin, M. B; Klein, E; Barry, C. E., 3rd and Flynn, J. L. Metronidazole prevents reactivation of latent Mycobacterium tuberculosis infection in macaques. Proc Natl Acad Sci USA. 109: 14188-14193. |  View Abstract

Fallahi-Sichani, M; Flynn, J. L; Linderman, J. J and Kirschner, D. E. Differential risk of tuberculosis reactivation among anti-TNF therapies is due to drug binding kinetics and permeability. J Immunol. 188: 3169-3178. |  View Abstract