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Choo, Min-Kyung

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Choo

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Min-Kyung

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Choo, Min-Kyung

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Author's Publications: search.filters.isAuthorOfPublication.8d7c4d94-bf1e-4fc3-8e9e-5c511d36ba00

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    Loss of Functionally Redundant p38 Isoforms in T Cells Enhances Regulatory T Cell Induction*
    (American Society for Biochemistry and Molecular Biology, 2017) Hayakawa, Morisada; Hayakawa, Hiroko; Petrova, Tsvetana; Ritprajak, Patcharee; Sutavani, Ruhcha V.; Jiménez-Andrade, Guillermina Yanek; Sano, Yasuyo; Choo, Min-Kyung; Seavitt, John; Venigalla, Ram K. C.; Otsu, Kinya; Georgopoulos, Katia; Arthur, J. Simon C.; Park, Jin Mo
    The evolutionarily conserved protein kinase p38 mediates innate resistance to environmental stress and microbial infection. Four p38 isoforms exist in mammals and may have been co-opted for new roles in adaptive immunity. Murine T cells deficient in p38α, the ubiquitously expressed p38 isoform, showed no readily apparent cell-autonomous defects while expressing elevated amounts of another isoform, p38β. Mice with T cells simultaneously lacking p38α and p38β displayed lymphoid atrophy and elevated Foxp3+ regulatory T cell frequencies. Double deficiency of p38α and p38β in naïve CD4+ T cells resulted in an attenuation of MAPK-activated protein kinase (MK)-dependent mTOR signaling after T cell receptor engagement, and enhanced their differentiation into regulatory T cells under appropriate inducing conditions. Pharmacological inhibition of the p38-MK-mTOR signaling module produced similar effects, revealing potential for therapeutic applications.
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    TLR sensing of bacterial spore-associated RNA triggers host immune responses with detrimental effects
    (The Rockefeller University Press, 2017) Choo, Min-Kyung; Sano, Yasuyo; Kim, Changhoon; Yasuda, Kei; Li, Xiao-Dong; Lin, Xin; Stenzel-Poore, Mary; Alexopoulou, Lena; Ghosh, Sankar; Latz, Eicke; Rifkin, Ian R.; Chen, Zhijian J.; Stewart, George C.; Chong, Hyonyong; Park, Jin Mo
    The spores of pathogenic bacteria are involved in host entry and the initial encounter with the host immune system. How bacterial spores interact with host immunity, however, remains poorly understood. Here, we show that the spores of Bacillus anthracis (BA), the etiologic agent of anthrax, possess an intrinsic ability to induce host immune responses. This immunostimulatory activity is attributable to high amounts of RNA present in the spore surface layer. RNA-sensing TLRs, TLR7, and TLR13 in mice and their human counterparts, are responsible for detecting and triggering the host cell response to BA spores, whereas TLR2 mediates the sensing of vegetative BA. BA spores, but not vegetative BA, induce type I IFN (IFN-I) production. Although TLR signaling in itself affords protection against BA, spore RNA–induced IFN-I signaling is disruptive to BA clearance. Our study suggests a role for bacterial spore–associated RNA in microbial pathogenesis and illustrates a little known aspect of interactions between the host and spore-forming bacteria.