Patricia Jones, Stanford University

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Professor Stanford, California patjones@stanford.edu Office: (650) 725-4818

Bio/Research

Dr. Jones' research has focused on genetic, molecular, and cellular mechanisms that regulate innate and adaptive immune responses. As immune responses can be harmful, they are highly regulated in their occurrence, magnitude, and duration. Her current work focuses on innate immune and inflammatory...

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Bio/Research

Dr. Jones' research has focused on genetic, molecular, and cellular mechanisms that regulate innate and adaptive immune responses. As immune responses can be harmful, they are highly regulated in their occurrence, magnitude, and duration. Her current work focuses on innate immune and inflammatory responses, triggered by conserved microbial components. Her research group discovered and is characterizing a novel mechanism that regulates innate responses of mammalian macrophages, dendritic cells, and other cells to microbial pathogens, resulting in generation of anti-microbial responses and production of cytokines and other proteins that contribute to innate, inflammatory, and adaptive immune responses. Dr. Jones' group discovered that the signaling pathways activated by the binding of microbial components to Toll-like receptors (TLR), leading to activation of the transcription factor NF-kB as well as MAPK pathways, is negatively-regulated by the protein phosphatase calcineurin. This inhibitory role of calcineurin, which helps to keep signaling downstream of TLR off in resting macrophages and other cells, is opposite to calcineurin's activating role in T and B lymphocytes following activation by antigen. Reflecting calcineurin's inhibitory role in macrophages, the signaling pathway downstream of TLR is activated by calcineurin inhibitors, such as cyclosporine A and FK506, that have long been used as immunosuppressants to block undesired T cell immune responses, such as those mediating organ transplant rejection.

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