The goal of this program is to provide pre-doctoral students with strong research training in specific basic science disciplines in combination with broad training in parasitology. Faculty members of this T32 have diverse basic science interests and study at least 11 different parasitic infections and most have a strong record of sustained NIH funding. There are several major research themes within this faculty that include immunity to parasitic infection as well as the area of cell, molecular, and developmental biology of parasites. These interests are the underlying core of our program. As a group, we also offer didactic training in parasitology and provide an environment in which students will gain an appreciation for broader aspects of parasitic disease research. The program at Penn has seen considerable growth in the last 10 years with the doubling in the numbers of active trainers from 6 to 15 and the increased pool of eligible students (>30). This proposal requests 6 slots for a period of five years to support graduate students performing their thesis studies. Relevance to Public Health: The numbers of individuals affected by parasitic diseases are difficult to gauge but even the most conservative estimates of the global impact of diseases caused by parasites are extraordinary. For example, almost half of the world's population live in malaria-endemic areas and every year 1 to 2 million people die of this disease. Two billion people on Earth are infected by soil-transmitted helminths and early childhood infections by these worms contribute significantly to slowing of physical and cognitive development. While the study of parasites is closely linked to many aspects of tropical medicine, this group of organisms also poses a serious public health problem in the developed world.

National Institute of Health (NIH)
National Institute of Allergy and Infectious Diseases (NIAID)
Institutional National Research Service Award (T32)
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Microbiology and Infectious Diseases B Subcommittee (MID)
Program Officer
Mcsweegan, Edward
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University of Pennsylvania
Schools of Veterinary Medicine
United States
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Novais, Fernanda O; Nguyen, Ba T; Beiting, Daniel P et al. (2014) Human classical monocytes control the intracellular stage of Leishmania braziliensis by reactive oxygen species. J Infect Dis 209:1288-96
Dupont, Christopher D; Christian, David A; Selleck, Elizabeth M et al. (2014) Parasite fate and involvement of infected cells in the induction of CD4+ and CD8+ T cell responses to Toxoplasma gondii. PLoS Pathog 10:e1004047
Liu, Weimin; Li, Yingying; Shaw, Katharina S et al. (2014) African origin of the malaria parasite Plasmodium vivax. Nat Commun 5:3346
Osborne, Lisa C; Monticelli, Laurel A; Nice, Timothy J et al. (2014) Coinfection. Virus-helminth coinfection reveals a microbiota-independent mechanism of immunomodulation. Science 345:578-82
Stoltzfus, Jonathan D; Bart, Stephen M; Lok, James B (2014) cGMP and NHR signaling co-regulate expression of insulin-like peptides and developmental activation of infective larvae in Strongyloides stercoralis. PLoS Pathog 10:e1004235
Kim, Brian S; Wang, Kelvin; Siracusa, Mark C et al. (2014) Basophils promote innate lymphoid cell responses in inflamed skin. J Immunol 193:3717-25
Millholland, Melanie G; Mishra, Satish; Dupont, Christopher D et al. (2013) A host GPCR signaling network required for the cytolysis of infected cells facilitates release of apicomplexan parasites. Cell Host Microbe 13:15-28
Geherin, Skye A; Lee, Michael H; Wilson, R Paul et al. (2013) Ovine skin-recirculating ýýýý T cells express IFN-ýý and IL-17 and exit tissue independently of CCR7. Vet Immunol Immunopathol 155:87-97
Saenz, Steven A; Siracusa, Mark C; Monticelli, Laurel A et al. (2013) IL-25 simultaneously elicits distinct populations of innate lymphoid cells and multipotent progenitor type 2 (MPPtype2) cells. J Exp Med 210:1823-37
Kim, Brian S; Siracusa, Mark C; Saenz, Steven A et al. (2013) TSLP elicits IL-33-independent innate lymphoid cell responses to promote skin inflammation. Sci Transl Med 5:170ra16

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