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Kelly J. Pittman

Researcher at Duke University

Publications -  17
Citations -  557

Kelly J. Pittman is an academic researcher from Duke University. The author has contributed to research in topics: Intracellular parasite & Chemokine. The author has an hindex of 10, co-authored 16 publications receiving 410 citations. Previous affiliations of Kelly J. Pittman include Georgia State University & University of Wisconsin-Madison.

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Dual transcriptional profiling of mice and Toxoplasma gondii during acute and chronic infection.

TL;DR: RNA-seq is a valuable tool to simultaneously analyze host and microbe transcriptomes and shows that T. gondii is metabolically active and synthesizing proteins at 28 days post-infection and that a distinct subset of host genes associated with the immune response are more abundant specifically during chronic infection.
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Long-Term Relationships: the Complicated Interplay between the Host and the Developmental Stages of Toxoplasma gondii during Acute and Chronic Infections

TL;DR: An overview of what is known and unknown about the complex relationship between the host and parasite during the progression of T. gondii infection is provided, with the ultimate goal of bridging these events.
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Salmonella Activation of STAT3 Signaling by SarA Effector Promotes Intracellular Replication and Production of IL-10.

TL;DR: RNA-seq of cells infected with either ΔsarA or wild-type S. Typhimurium revealed that SarA activates STAT3 transcriptional targets and contributes to intracellular replication in vitro and bacterial load at systemic sites in mice, demonstrating that Salmonella has evolved mechanisms for activating an important anti-inflammatory pathway.
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An Atlas of Genetic Variation Linking Pathogen-Induced Cellular Traits to Human Disease.

TL;DR: The Hi-HOST Phenome Project (H2P2) is reported, a catalog of cellular genome-wide association studies (GWAS) comprising 79 infection-related phenotypes in response to 8 pathogens in 528 lymphoblastoid cell lines and a SNP in the transcriptional repressor ZBTB20 demonstrated pleiotropy, likely through suppression of multiple target genes, and was associated with viral hepatitis.