M
Michael Carty
Researcher at Trinity College, Dublin
Publications - 17
Citations - 1264
Michael Carty is an academic researcher from Trinity College, Dublin. The author has contributed to research in topics: Innate immune system & Pattern recognition receptor. The author has an hindex of 10, co-authored 17 publications receiving 965 citations.
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The human adaptor SARM negatively regulates adaptor protein TRIF-dependent Toll-like receptor signaling
TL;DR: The fifth mammalian TIR adaptor SARM is a negative regulator of Toll-like receptor signaling, and 'knockdown' of endogenous SARM expression by interfering RNA led to enhanced TRIF-dependent cytokine and chemokine induction.
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Detection of Viral Infections by Innate Immunity.
TL;DR: Recent insights into the influence of PRR activation and inflammasomes on viral infections and what this means for the mammalian host are discussed.
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Evaluating the role of Toll-like receptors in diseases of the central nervous system.
Michael Carty,Andrew G. Bowie +1 more
TL;DR: This review aims to examine the recent literature on TLRs in the CNS thus demonstrating their importance in a range of infectious and non-infectious diseases of the brain.
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Recent insights into the role of Toll‐like receptors in viral infection
Michael Carty,Andrew G. Bowie +1 more
TL;DR: Earlier evidence, mainly from knock‐out mice studies, implicating TLRs in the innate immune response to viruses are discussed in light of more recent clinical data demonstrating that TLRs are important for anti‐viral immunity in humans.
Journal ArticleDOI
Cell Survival and Cytokine Release after Inflammasome Activation Is Regulated by the Toll-IL-1R Protein SARM
Michael Carty,Jay Kearney,Katharine A. Shanahan,Emily Hams,Ryoichi Sugisawa,Dympna J. Connolly,Ciara G. Doran,Natalia Muñoz-Wolf,Claudia Gürtler,Katherine A. Fitzgerald,Ed C. Lavelle,Padraic G. Fallon,Andrew G. Bowie +12 more
TL;DR: SARM-dependent mitochondrial depolarization distinguishes NLRP3 activators that cause pyroptosis from those that do not, and SARM modulation represents a cell-intrinsic mechanism to regulate cell fate after inflammasome activation.