J
Jonathan P. Richardson
Researcher at King's College London
Publications - 56
Citations - 3455
Jonathan P. Richardson is an academic researcher from King's College London. The author has contributed to research in topics: Candida albicans & Candidalysin. The author has an hindex of 27, co-authored 50 publications receiving 2572 citations. Previous affiliations of Jonathan P. Richardson include University College London & University of Manchester.
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Journal ArticleDOI
Candidalysin is a fungal peptide toxin critical for mucosal infection
David L. Moyes,Duncan Wilson,Jonathan P. Richardson,Selene Mogavero,Shirley X. Tang,Julia Wernecke,Sarah Höfs,Remi L. Gratacap,Jon Robbins,Manohursingh Runglall,Celia Murciano,Mariana Blagojevic,Selvam Thavaraj,Toni M. Förster,Betty Hebecker,Lydia Kasper,Gema Vizcay,Simona Ioana Iancu,Nessim Kichik,Nessim Kichik,Antje Häder,Oliver Kurzai,Ting Luo,Thomas Krüger,Olaf Kniemeyer,Ernesto Cota,Oliver Bader,Robert T. Wheeler,Thomas Gutsmann,Bernhard Hube,Julian R. Naglik +30 more
TL;DR: A fungal cytolytic peptide toxin in the opportunistic pathogen Candida albicans was identified in this article, which directly damages epithelial membranes, triggers a danger response signalling pathway and activates epithelial immunity.
Candidalysin is a Fungal Peptide Toxin Critical for Mucosal Infection and Immune Activation
TL;DR: This work identifies the first, to the authors' knowledge, fungal cytolytic peptide toxin in the opportunistic pathogen Candida albicans, which directly damages epithelial membranes, triggers a danger response signalling pathway and activates epithelial immunity.
Journal ArticleDOI
Endless possibilities: translation termination and stop codon recognition
TL;DR: A review of recent advances in the use of optimized, complex, reconstituted in vitro termination reactions to identify the roles of key termination factors, and the solution of tertiary structures of termination factors has allowed a reappraisal of termination factor structure and function.
Journal ArticleDOI
Oral epithelial cells orchestrate innate type 17 responses to Candida albicans through the virulence factor candidalysin.
Akash H. Verma,Jonathan P. Richardson,Chunsheng Zhou,Bianca M. Coleman,David L. Moyes,J. Ho,Anna R. Huppler,Kritika Ramani,Mandy J. McGeachy,Ilgiz A. Mufazalov,Ari Waisman,Lawrence P. Kane,Partha S. Biswas,Bernhard Hube,Bernhard Hube,Julian R. Naglik,Sarah L. Gaffen +16 more
TL;DR: It is proposed that the innate antifungal responses to C. albicans are driven by a synergy between cellular damage triggered by candidalysin that is further amplified by interleukin-17 driven inflammation, and establishment of IL-1– and IL-17–dependent innate immunity is induced by tissue-damaging hyphae.
Journal ArticleDOI
IL-17 Receptor Signaling in Oral Epithelial Cells Is Critical for Protection against Oropharyngeal Candidiasis.
Heather R. Conti,Heather R. Conti,Vincent M. Bruno,Erin E. Childs,Sean C. Daugherty,Joseph P. Hunter,Bemnet G. Mengesha,Danielle La Saevig,Matthew R. Hendricks,Bianca M. Coleman,Lucas Brane,Norma V. Solis,J. Agustin Cruz,Akash H. Verma,Abhishek V. Garg,Amy G. Hise,Amy G. Hise,Jonathan P. Richardson,Julian R. Naglik,Scott G. Filler,Jay K. Kolls,Satrajit Sinha,Sarah L. Gaffen,Sarah L. Gaffen +23 more
TL;DR: OECs dominantly control IL-17R-dependent responses to OPC through regulation of BD3 expression, and Susceptibility in Il17raΔK13 mice correlated with expression of the antimicrobial peptide β-defensin 3 (BD3, Defb3).