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Invasive fungal infections are a leading cause of death among immunocompromised patients. It is therefore essential to define the cellular and molecular mechanisms of host-pathogen interactions in order to improve outcomes for patients with invasive fungal infections. At the Vyas Laboratory in the Infectious Diseases Division of Massachusetts General Hospital, our research interests lie at the intersection between pathogenic fungal organisms and the immune system.
The first line of defense against these pathogens is phagocytic cells including neutrophils, macrophages, and dendritic cells. Once phagocytes recognize and engulf fungal pathogens, they are placed into membrane-delimited compartments termed phagosomes. In a process known as phagosome maturation, ingested materials are trafficked through a series of increasingly acidified structures, ultimately leading to the degradation of the pathogen. The Vyas Lab uses fungal pathogens of clinical importance including Cryptococcus neoformans, Aspergillus fumigatus and Candida albicans as the model pathogens to study phagosome formation and maturation. Using live cell imaging and fluorescently-tagged proteins, we visualize primary macrophages and their responses to fungi. We examine the role of pattern-recognition receptors such as Dectin-1 and Toll-like receptors in fungal immunity. We are also interested in the role of LC-3 (member of the autophagy family of proteins) and members of the tetraspanin family and their effects on phagosomal maturation. Knowledge gained understanding these molecular events will hopefully tailor the immune response to these clinically relevant fungal pathogens in immunocompromised patients.
- Khan NS, Kasperkovitz PV, Timmons AK, Mansour MK, Tam JM, Seward MW, Reedy JL, Puranam S, Feliu M, and Vyas JM(2016). Dectin-1 Controls TLR9 Trafficking to Phagosomes Containing beta-1,3 Glucan. J Immunol. 196(5):2249-61.
- Tam, J.M., Mansour, M.K., Acharya, Sokolovska, A, M., Timmons, A.K., Lacy-Hulbert, A., and Vyas, J.M. (2016). The role of autophagy-related proteins in C. albicans infection. Pathogens. 5 (2)
- Tam, J.M., Mansour, M.K., Khan, N.S., Seward, M., Puranam, S., Tanne, A., Sokolovska, A., Becker, C.E., Acharya, M., Baird, M.A., Choi, A.M., Davidson, M.W., Segal, B.H., Lacy-Hulbert, A., Stuart, L.M., Xavier, R.J., and Vyas, J.M. (2014). Dectin-1-dependent LC3 recruitment to phagosomes enhances fungicidal activity in macrophages. J Infect Dis 210, 1844-1854.
- Mansour, M.K., Reedy, J.L., Tam, J.M., and Vyas, J.M. (2014). Macrophage Cryptococcus interactions: an update. Curr Fungal Infect Rep 8, 109-115.
- Mansour, M.K., Tam, J.M., Khan, N.S., Seward, M., Davids, P.J., Puranam, S., Sokolovska, A., Sykes, D.B., Dagher, Z., Becker, C., Tanne, A., Reedy, J.L., Stuart, L.M., and Vyas, J.M. (2013). Dectin-1 activation controls maturation of beta-1,3-glucan-containing phagosomes. J Biol Chem 288, 16043-16054.
- Mansour, M.K., Tam, J.M., and Vyas, J.M. (2012). The cell biology of the innate immune response to Aspergillus fumigatus. Ann N Y Acad Sci 1273, 78-84.
- Tam, J.M., Mansour, M.K., Khan, N.S., Yoder, N.C., and Vyas, J.M. (2012). Use of fungal derived polysaccharide-conjugated particles to probe Dectin-1 responses in innate immunity. Integr Biol (Camb) 4, 220-227.
- Vyas, J.M. (2012). The dendritic cell: the general of the army. Virulence 3, 601-602.
- Vyas, J.M. (2012). Insights into dendritic cell function using advanced imaging modalities. Virulence 3, 690-694.
- Artavanis-Tsakonas, K., Kasperkovitz, P.V., Papa, E., Cardenas, M.L., Khan, N.S., Van der Veen, A.G., Ploegh, H.L., and Vyas, J.M. (2011). The tetraspanin CD82 is specifically recruited to fungal and bacterial phagosomes prior to acidification. Infect Immun 79, 1098-1106.
- Tam, J.M., Castro, C.E., Heath, R.J., Mansour, M.K., Cardenas, M.L., Xavier, R.J., Lang, M.J., and Vyas, J.M.(2011). Use of an optical trap for study of host-pathogen interactions for dynamic live cell imaging. J Vis Exp.
- Vyas, J.M. (2011). The duality of Aspergillus terreus: Differential immune responses to distinct conidia.Virulence 2, 181-184.
- Kasperkovitz, P.V., Cardenas, M.L., and Vyas, J.M. (2010). TLR9 is actively recruited to Aspergillus fumigatus phagosomes and requires the N-terminal proteolytic cleavage domain for proper intracellular trafficking. J Immunol 185, 7614-7622.
- Tam, J.M., Castro, C.E., Heath, R.J., Cardenas, M.L., Xavier, R.J., Lang, M.J., and Vyas, J.M. (2010). Control and manipulation of pathogens with an optical trap for live cell imaging of intercellular interactions. PLoS One 5, e15215.
- Artavanis-Tsakonas, K., Love, J.C., Ploegh, H.L., and Vyas, J.M. (2006). Recruitment of CD63 to Cryptococcus neoformans phagosomes requires acidification. Proc Natl Acad Sci U S A 103, 15945-15950.
Jatin M. Vyas, MD, PhD is an Associate Professor of Medicine at Harvard Medical School and the Internal Medicine Residency Program Director at Massachusetts General Hospital. Learn more about him and the rest of the research group.
Jenny M. Tam, PhD
Instructor in Medicine, Harvard Medical School
Assistant in Immunology, Massachusetts General Hospital
Jennifer L. Reedy, MD, PhD
Instructor in Medicine, Harvard Medical School
Allison Timmons, PhD
Nida S. Khan
Research Technician II