seth masters
@sethmasters
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Head of the Centre for Innate Immunity and Infectious Diseases, Hudson Institute.
Melbourne, Australia
Joined February 2009
Monogenic autoinflammatory diseases tended to be defined by specific cytokines, such as IL-1b, IL-6, TNF and type I IFN. However, the condition APLAID did not fit, and instead we find that it may be the first of a new category that are caused by G-CSF.
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Dear Everyone, I've read the #NHMRC draft strategy and I have notes ... So I'm going to...🧵🤔🧵😱🧵😵💫🧵🙏🧵🧵🧵 #NHMRCdraftStratergy #Ihavenotes #ValueFundamentalScience
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🔊 🗓️ SAVE THE DATE ASI Innate Immunity SIG and Australian Inflammation Centres as well as Australasian Cell Death Society jointly host a symposium on 10-11 Nov at the University of Adelaide. More details to come. #ASImmunology
#innateimmunity #inflammation #celldeath
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Amazing work by first author @shouya_feng with the support of many others, thanks all!!!
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We tested this library of NLRP3 variants in response to stimulation, at low temperature (some patients with CAPS have temperature sensitive flares), and in response to a NLRP3 inhibitor, all of which yielded interesting results. If you have another idea, we are happy to share!
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Data available through https://t.co/YAA37HDqCb and https://t.co/dPWkaRvnBu any variants we did not test yet please let me know!
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A large dataset we hope is helpful for patients who may have CAPS, an #autoinflammatory condition associated with gene variants in NLRP3. Many variants of uncertain significance now have a readout from our in vitro assay which can aid clinical diagnosis.
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A starter pack for anyone interested in #autoinflammation and #autoinflammatory diseases. Please let me know if you’d like to be added. https://t.co/m6y9J4INl2
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Most certainly in my calendar! Miss this chance and the next one is not till 2027!
We are delighted to invite you to the 13th Meeting of the International Society of Systemic Autoinflammatory Diseases (ISSAID), which will take place in Paris from April 8th to 10th, 2025. ▶️ https://t.co/xGuJVs2izl
@HelenLachmann @AAlliance_SAID @_ERNRITA @contactfai2r
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Come along to our #StudentOpenDay & take your research degree in biomedicine & clinical sciences to the next level Thurs 15th August 5-7pm Auditorium, Level 4, Green Chemical Futures Building, 13 Rainforest Walk, Monash University, Main Clayton Campus ➡️ https://t.co/vlAbr2gfhp
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Also! I'm recruiting for a... Post doc: https://t.co/iBpRHBBXTb And an RA: https://t.co/eaVOhEVLWQ If you're interested in discovering weird and wonderful triggers of inflammation in #neurodevelopmentaldisorder, #neurodegeneration and #inflammatorydisease please apply
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Our laboratory is hiring at the Postdoc or RA level! If Innate Immunology and Autoinflammatory Disease are of interest to you consider to join us @Hudson_Research in Melbourne Australia! https://t.co/crtqqlfhqB
https://t.co/9wFAhkjJGk
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TLDR - associated "Research Briefing" for our article.
nature.com
Nature Immunology - This work identifies two rare genetic variants of UNC93B1 that contribute to the development of childhood-onset lupus. Mice that expressed one of these variants developed a...
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UNC93B1 variants don't seem very spontaneously active - Tend to be hyper-responsive to TLR7/8, would blocking a single TLR in vivo be therapeutic? - Is there an endogenous or infectious trigger? - Different mutations, different mechanisms?
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We found mutations in UNC93B1 can cause early-set lupus, also reported by @barton_lab Min Ae Lee-Kirsch @MajerOlivia and colleagues, likely many more patients yet to be diagnosed. https://t.co/uH08SCG6YR
nature.com
Nature Immunology - Rare genetic variants in UNC93B1 predispose to childhood-onset lupus via TLR7/-8–IRAK1/-4, validated with a corresponding mouse model.
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IL-18 as a contributor to renal involvement in lupus-like disease, an interesting proposal based on an NLRC4 Gain-of-Function Mutation by @AlexandreBelot and colleagues
kireports.org
NLRC4 belongs to the family of innate immunity receptors. These receptors have the ability to detect microbial patterns and molecular signals of cellular damage within the cell. The involvement of...
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There was one big update in this publication by @science_sophie since the preprint - a second patient with the same dominant negative mutation in Otulin, contributed by @jqanatish and others from the King Abdullah Children’s Hospital in Riyadh. 🙏 all!
In @JExpMed, Davidson, Shibata, @komander_lab @sethmasters @WEHI_research et al identify a novel dominant negative heterozygous mutation in OTULIN (p.Cys129S) that enhances cell death & inflammatory signaling, thereby driving autoinflammatory disease. https://t.co/z2abAvjRPb
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No surprise I can't remember those TLR9 siRNA experiments... https://t.co/fzVZkgb0hC
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The registration website for our upcoming Inflammasome EMBO Workshop on September 24-27, 2024 is now live. Check out the fantastic line-up of speakers who will be joining us 🤩. Also, lots of opportunities for short talks available! https://t.co/Ju8QQasOfx
meetings.embo.org
The innate branch of the immune system serves as the first line of defense that has the intricate task to detect molecules and organisms that are of danger to the organism. Inflammasomes constitute a…
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We have an open Melbourne-based #PhD position in the @sethmasters lab @Hudson_Research & the @IsbBonn @UniBonn. The project focusses on the role of the inflammasome in the context of autoinflammatory diseases. For more info see👉 https://t.co/cYn0ZWb6Ky
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Our world leading #Inflammation programs enter a new era with the appointment of Prof @sethmasters to lead the Centre for Innate Immunity & Infectious Diseases (@CiiiD_Hudson)! 👏🏽
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