K
Kingston H. G. Mills
Researcher at Trinity College, Dublin
Publications - 326
Citations - 33937
Kingston H. G. Mills is an academic researcher from Trinity College, Dublin. The author has contributed to research in topics: Immune system & Bordetella pertussis. The author has an hindex of 92, co-authored 313 publications receiving 29630 citations. Previous affiliations of Kingston H. G. Mills include The Hertz Corporation & Maynooth University.
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Journal ArticleDOI
A small-molecule inhibitor of the NLRP3 inflammasome for the treatment of inflammatory diseases
Rebecca C. Coll,Avril A. B. Robertson,Jae Jin Chae,Sarah C. Higgins,Raúl Muñoz-Planillo,Marco Inserra,Irina Vetter,Lara S. Dungan,Brian G. Monks,Andrea Stutz,Daniel E. Croker,Mark S. Butler,Moritz Haneklaus,Caroline E. Sutton,Gabriel Núñez,Eicke Latz,Daniel L. Kastner,Kingston H. G. Mills,Seth L. Masters,Kate Schroder,Mark E. Cooper,Luke A. J. O'Neill +21 more
TL;DR: MCC950 treatment rescued neonatal lethality in a mouse model of CAPS and was active in ex vivo samples from individuals with Muckle–Wells syndrome, and is a potential therapeutic for NLRP3-associated syndromes, and a tool for further study of theNLRP3 inflammasome in human health and disease.
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Trained immunity: A program of innate immune memory in health and disease
Mihai G. Netea,Leo A. B. Joosten,Eicke Latz,Kingston H. G. Mills,Gioacchino Natoli,Hendrik G. Stunnenberg,Luke A. J. O'Neill,Ramnik J. Xavier +7 more
TL;DR: Proof-of-principle experimental studies support the hypothesis that trained immunity is one of the main immunological processes that mediate the nonspecific protective effects against infections induced by vaccines, such as bacillus Calmette-Guérin or measles vaccination.
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Interleukin-1 and IL-23 induce innate IL-17 production from gammadelta T cells, amplifying Th17 responses and autoimmunity.
Caroline E. Sutton,Stephen J. Lalor,Cheryl M. Sweeney,Corinna F. Brereton,Ed C. Lavelle,Kingston H. G. Mills +5 more
TL;DR: It is shown that gammadelta T cells express IL-23R and the transcription factor RORgammat and produce IL-17, IL-21, and IL-22 in response to IL-1beta andIL-23, without T cell receptor engagement.
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Activation of the NLRP3 inflammasome by islet amyloid polypeptide provides a mechanism for enhanced IL-1β in type 2 diabetes
Seth L. Masters,Aisling Dunne,Shoba L. Subramanian,Rebecca L. Hull,Gillian M. Tannahill,Fiona A. Sharp,Christine Becker,Luigi Franchi,Eiji Yoshihara,Zhe Chen,Niamh Mullooly,Lisa A. Mielke,James Harris,Rebecca C. Coll,Kingston H. G. Mills,K. Hun Mok,Philip Newsholme,Gabriel Núñez,Junji Yodoi,Steven E. Kahn,Ed C. Lavelle,Luke A. J. O'Neill +21 more
TL;DR: It is shown that oligomers of islet amyloid polypeptide (IAPP), a protein that formsAmyloid deposits in the pancreas during type 2 diabetes, triggered the NLRP3 inflammasome and generated mature IL-1β.
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A crucial role for interleukin (IL)-1 in the induction of IL-17–producing T cells that mediate autoimmune encephalomyelitis
TL;DR: IL-1 functions upstream of IL-17 to promote pathogenic ThIL-17 cells in EAE, and essential roles for phosphatidylinositol 3-kinase, nuclear factor κB, and novel protein kinase C isoforms in IL-1– and IL-23–mediated IL- 17 production are demonstrated.