H
Hazel Tye
Researcher at Walter and Eliza Hall Institute of Medical Research
Publications - 14
Citations - 1603
Hazel Tye is an academic researcher from Walter and Eliza Hall Institute of Medical Research. The author has contributed to research in topics: Innate immune system & Inflammation. The author has an hindex of 11, co-authored 12 publications receiving 1242 citations. Previous affiliations of Hazel Tye include Monash Institute of Medical Research & Monash University, Clayton campus.
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Journal ArticleDOI
STAT3 and STAT1 mediate IL-11–dependent and inflammation-associated gastric tumorigenesis in gp130 receptor mutant mice
Matthias Ernst,Meri Najdovska,Dianne Grail,Therese Lundgren-May,Michael Buchert,Hazel Tye,Vance Matthews,Jane E. Armes,Prithi S. Bhathal,Norman R. Hughes,Eric G. Marcusson,James G. Karras,Songqing Na,Jonathon D. Sedgwick,Paul J. Hertzog,Brendan J. Jenkins +15 more
TL;DR: IL-11 was identified as a crucial cytokine promoting chronic gastric inflammation and associated tumorigenesis mediated by excessive activation of STAT3 and STAT1 and reducing STAT3 activity in gp130F/Y757F mice, normalized gastric IL-11 expression and alleviated gastric tumor burden.
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Germline NLRP1 Mutations Cause Skin Inflammatory and Cancer Susceptibility Syndromes via Inflammasome Activation
Franklin L. Zhong,Ons Mamaï,Lorenzo Sborgi,Lobna Boussofara,Richard Hopkins,Kim S. Robinson,Ildikó Szeverényi,Takuya Takeichi,Takuya Takeichi,Reshmaa Balaji,Aristotle Lau,Hazel Tye,Hazel Tye,Keya Roy,Carine Bonnard,Patricia J. Ahl,L. A. Jones,Paul J. Baker,Paul J. Baker,Lukáš Lacina,Atsushi Otsuka,Pierre Fournié,François Malecaze,E. Birgitte Lane,Masashi Akiyama,Kenji Kabashima,Kenji Kabashima,John E. Connolly,Seth L. Masters,Seth L. Masters,Vincent Soler,Salma Samir Omar,John A. McGrath,Roxana Ioana Nedelcu,Moez Gribaa,Mohamed Denguezli,Ali Saad,Sebastian Hiller,Bruno Reversade +38 more
TL;DR: It is found that germline mutations in the inflammasome sensor NLRP1 cause two overlapping skin disorders: multiple self-healing palmoplantar carcinoma (MSPC) and familial keratosis lichenoides chronica (FKLC) and the first genetic evidence linkingNLRP1 to skin inflammatory syndromes and skin cancer predisposition is provided.
Journal ArticleDOI
Myeloid-derived miR-223 regulates intestinal inflammation via repression of the NLRP3 inflammasome
Viola Neudecker,Viola Neudecker,Moritz Haneklaus,Owen Jensen,Ludmila Khailova,Joanne C. Masterson,Joanne C. Masterson,Hazel Tye,Hazel Tye,Kathryn A. Biette,Kathryn A. Biette,Paul Jedlicka,Kelley S. Brodsky,Mark E. Gerich,Matthias Mack,Avril A. B. Robertson,Mark E. Cooper,Glenn T. Furuta,Glenn T. Furuta,Charles A. Dinarello,Charles A. Dinarello,Luke A. J. O'Neill,Holger K. Eltzschig,Holger K. Eltzschig,Seth L. Masters,Seth L. Masters,Eóin N. McNamee +26 more
TL;DR: It is reported that miR-223 limits intestinal inflammation by constraining the nlrp3 inflammasome in mice, revealing a previously unappreciated role in regulating the innate immune response during intestinal inflammation.
Journal ArticleDOI
STAT3-Driven Upregulation of TLR2 Promotes Gastric Tumorigenesis Independent of Tumor Inflammation
Hazel Tye,Catherine Kennedy,Meri Najdovska,Louise McLeod,William McCormack,Norman R. Hughes,Anouk Dev,William Sievert,Chia Huey Ooi,Tomo-o Ishikawa,Hiroko Oshima,Prithi S. Bhathal,Andrew E. Parker,Masanobu Oshima,Patrick Tan,Patrick Tan,Brendan J. Jenkins +16 more
TL;DR: An unexpected role for TLR2 in the oncogenic function of STAT3 that may represent a therapeutic target in GC is revealed.
Journal ArticleDOI
Aberrant actin depolymerization triggers the pyrin inflammasome and autoinflammatory disease that is dependent on IL-18, not IL-1β
Man Lyang Kim,Jae Jin Chae,Yong Hwan Park,Dominic De Nardo,Roslynn A. Stirzaker,Hyun-Ja Ko,Hazel Tye,Louise H. Cengia,Ladina DiRago,Donald Metcalf,Andrew W. Roberts,Daniel L. Kastner,Andrew M. Lew,Dena Lyras,Benjamin T. Kile,Ben A. Croker,Seth L. Masters +16 more
TL;DR: An autoinflammatory disease in mice is identified, resulting from an inactivating mutation in the actin-depolymerizing cofactor Wdr1, resulting in exaggerated monocyte IL-18 production, whereas inflammasome activation in mature macrophages is unaltered.