Kate Lawlor

Enteropathogenic bacteria evade ROCK-driven epithelial cell extrusion - Nature The bacterial ubiquitin ligase NleL evades host defence mechanisms both by inhibiting pyroptosis and by preventing infected intestinal epithelial cells from being extruded into the lumen and expelled ...

#EveryCellIsAnImmuneCell! Luchetti @rauchlab.bksy.social Dixit &co show @nature.com that enteropathogenic bacteria evolved a virulence factor that degrades non-canonical #inflammasome & targets ROCKs necessary for luminal extrusion of infected intestinal #epithelial cells, favoring bacterial growth!

Open Group Leader Positions at the IMB, UQ. Interested in joining us in sunny Queensland?

Cardiolipin inhibits the non-canonical inflammasome by preventing LPS binding to caspase-4/11 | The EMBO Journal imageimageAvailable caspase-4/11 (CASP4/11) inhibitors also block the activity of caspase-1 (CASP1), which complicates interpretation of results in functional studies and limits their clinical potenti...

Congrats to @malvinapiz.bsky.social and @inflammasomelab.bsky.social on their new paper on the role of cardiolipin in non canonical inflammasome activation. We’re happy to have contributed to the story 🎉🦠!!

www.embopress.org/doi/full/10....

Potentiating cancer immunotherapies with modular albumin-hitchhiking nanobody–STING agonist conjugates - Nature Biomedical Engineering A modular anti-albumin nanobody conjugated to a STING agonist enhances antitumour immunity by improving pharmacokinetics, tumour accumulation and immune responses, inhibiting murine tumour growth and ...

A small-molecule STING agonist is conjugated to a nanobody that binds to serum albumins to increase tumor accumulation and augment antitumor immunity
www.nature.com/articles/s41...
www.nature.com/articles/s41...

No budget increase for the Australian Research Council 😡

Congrats Michelle, @kaiwenchen-lab.bsky.social and team

I’m happy to share that my first first-author publication is now out! 🎉

Enteric tuft cell inflammasome activation drives NKp46+ILC3 IL22 via PGD2 and inhibits Salmonella PGD2 released after NAIP-NLRC4 inflammasome activation in tuft cells signals onto ILC3s and mediates host defense mechanisms against Salmonella Typhimurium

#WeekendRead! #InflammasomePower! @rauchlab.bsky.social &co show @jem.org that small intestinal tufts cells activate the NLRC4 inflammasome leading to PGD2-dependent IL-22 production by ILC3, protecting against Salmonella!
rupress.org/jem/article/...

MARCO is an IFN-restricted immunometabolic decoy LPS receptor Intracellular sensing of lipopolysaccharide is an essential component of pathogen detection that governs the innate immune response. However, how this process is controlled to maintain homeostasis and...

Sharing my labs first pre-print ! We discovered a remarkable innate checkpoint in macrophages ! Congrats to tall the authors @umassmedicine.bsky.social @umasschan.bsky.social

www.biorxiv.org/content/10.1...

This is amazing!!!

We are recruiting a group leader in laboratory research at Peter Mac Cancer Centre in
Melbourne, Australia 🔬🦘💥

Work in a cutting edge research environment in a vibrant world city!

We value research excellence, creativity and diversity.

Join us!

careers.petermac.org/job/MELBOURN...

NHMRC Investigator grant success 2025 Research into autoinflammatory diseases, hypertension, cancer and perinatal brain injury has been funded by NHMRC Investigator grants.

I am incredibly fortunate and delighted to have been awarded a NHMRC Emerging Leadership Level 1 Investigator Grant this year! 🥳 This funding will provide crucial support for my research on interferon epsilon in cancer over the next 5 years. @hudsonresearch.bsky.social #nhmrc #investigatorgrant

Table from page 25 of the proposed restructure of ARC grants. Back text on white background, with the table delineated by a dark blue header row and alternating light and very light blue rows.

The ARC Board has proposed a major shake-up of the National Competitive Grants Program ▶️ www.arc.gov.au/engage-us/co...

I've only skimmed so far, but they propose reducing 13 grant schemes to 6, with intent & scope in the table👇

Submissions are being accepted in response until 13 April. Get to it!

Excited to share our latest preprint! We find that DCs undergo heterogeneous cell death- either pyroptosis or apoptosis upon bacterial blockade of host translation- to restrict Legionella infection. Congrats to my PhD student @vvazquez.bsky.social & co-authors! Check out his bluetorial 🧵 below! 👇

Would love to talk to ECRs who might be interested in applying for a post-doctoral fellowship to study human inflammasomes! The Royal Society Newton International Fellowships are open to anyone outside the UK. More details in the post below

Confirmed speakers:
A. Ablasser
L. Andreeva
@audeber.bsky.social
@jelenalab.bsky.social
V. Dixit
@v-hornung.bsky.social
B. Lemaitre
O. Majer
@manellab.bsky.social
E. Miao
@oliveiramann.bsky.social
M. Pasparakis
@inflammasomelab.bsky.social
@sparrerlab.bsky.social
R. Vance
@lozanzi.bsky.social

Sterile- or pathogen-induced endolysosomal damage activate the NLRP6 inflammasome in human intestinal epithelial cells NLRP6 controls host defense against bacteria and viruses in the gastrointestinal tract by a poorly understood mechanism. Here, we report that NLRP6 forms an inflammasome upon endolysosomal damage caus...

Check out our latest pre print! Alexandra and colleagues show that the enigmatic inflammasome receptor, NLRP6 is activated by sterile and pathogen induced endolysosomal damage. Hot off the press!

www.biorxiv.org/content/10.1...

The TLR7/9 adaptors TASL and TASL2 mediate IRF5-dependent antiviral responses and autoimmunity in mouse - Nature Communications TASL is an adaptor molecule bridging Toll-like receptor signalling and transcription activation by IRF5. Here the authors show that TASL deficiency impacts TLR7/9 responses, and that a TASL paralogue,...

Excited to share our latest paper out today in @naturecomms.bsky.social !

Great work led by postdoc Ales Drobek showing for the first time the critical role in vivo of the SLC15A4/TASL/IRF5 pathway that we discovered few years ago.

#ImmunoSky #InterferoSky

Antigen-presenting cell activation requires intrinsic and extrinsic STING signaling after the phagocytosis of DNA-damaged cells Both cytosolic DNA species and innate immune STING signaling are required for stressed cells to activate phagocytes.

#WeekendRead! #EveryCellisAnImmuneCell! Park, Ahn & Barber show @sciimmunology.bsky.social that DNA-damaged cells activate cGAS-STING secreting factors & induce endosomal vesicles that activate in antigen-presenting cells cGAS-STING inducing immune activation! www.science.org/doi/10.1126/...

Cellular RNA interacts with MAVS to promote antiviral signaling Antiviral signaling downstream of RIG-I–like receptors (RLRs) proceeds through a multi-protein complex organized around the adaptor protein mitochondrial antiviral signaling protein (MAVS). Protein co...

#InterferonPower! Fantastic @science.org by @nandangokhale.bsky.social @ramlabuw.bsky.social &co! MAVS is intrinsically capable to sense via an unstructured region the 3’ UTRs of self mRNA (ISGs too!) to potentiate the response to viral RNA via phosphorylation of IRF3 & NFkB!

Ever wondered how gut microbes control immune responses at extra-intestinal locations?
Here #theonlylabever reports how a gut protozoan commensal shapes pulmonary immunity to exacerbate asthma and limit the dissemination of mycobacteria.
@cellpress.bsky.social ⬇️(1/x)
www.cell.com/cell/fulltex...

Are you a strong leader who wants to make a difference in cancer research? Become part of a dynamic, forward-thinking leadership team @onjcri.org.au and contribute to groundbreaking work that improves the lives of cancer patients. www.onjcri.org.au/join-our-tea...

#InterferonPower! #NotAllIFNsAreEqual! Casanova, Zhang, Al Qureshah &co show @jexpmed.bsky.social that a common (in China) autosomal dominant IFNAR1 variant impairs -not abolishes- IFN-alpha & -omega (not -beta!) responses making patients susceptible to some -not all- viruses doi.org/10.1084/jem....

@onjcri.org.au is seeking a visionary Chief Scientific Research Officer (CSRO) to lead cutting-edge cancer research. If you have the qualifications and passion to make a real impact, don’t miss this chance! Submit your EOI here: www.onjcri.org.au/recruitment/...

#CancerResearch #Anticancer

Happy to share our latest preprint from 1st author & PhD student @vvazquez.bsky.social examining how GM-CSF potentiates cytokine responses in human monocytes during bacterial infection! Congrats to Victor, his undergrad mentees Allyson Lu & Madison Dresler, & postdoc @mikelhaggadone.bsky.social! 🧪

The inflammatory microenvironment of the lung at the time of infection governs innate control of SARS-CoV-2 replication Recent or ongoing respiratory inflammation in the lung regulates antiviral immune responses to SARS-CoV-2.

Excited to share this paper from my post-doc at @niaidnews.bsky.social out now in Science Immunology! We show that recent or ongoing 🫁 infections or other pulmonary environmental exposures at the time of infection with SARSCoV2 can vastly influence early replication of the virus in mice.

Graphical summary of our paper. In mice, prior lower airway exposure to diverse inflammatory stimuli, including chronic bacterial infections such as M. tuberculosis, acute bacterial infections such as pulmonary S. aureus, viral infections such as Influenza A, type-II allergic responses such as the OVA-Alum model, activation of pulmonary TLR9 by CpG or pulmonary TLR1/2 by Pam3CSK4 leads to reduced viral burden upon subsequent infection with SARS-CoV-2 (SCV2). (2) This SCV2 restriction occurs prior to induction of SCV2-specific adaptive immune responses and is mediated through innate immune responses, including the induction of IFN-I, TNFα and IL-1 and sustained changes to the TRM (Tissue resident macrophage) cellular compartment and the pulmonary epithelium. (3) Innate cytokine and TLR signaling to both recruited immune cells and the pulmonary epithelium creates a microenvironment in the lung that limits early replication of SCV2. IFN-I signaling to pulmonary ECs (epithelial cells) increases expression of interferon-stimulated genes, that likely cell-intrinsically limit viral replication. TNF- or IL-1 suppress SCV2 independently of IFN-I signaling. TNF acts exclusively through radio-resistant cell types such as the lung epithelium, whereas IL-1 affords control both direct and indirectly, through either stromal and hematopoietic cell types, to restrict overall early SCV2 burden.

Best #Nikolaus 🎅! Our paper on how the 🫁 microenvironment can shape #innate immunity against #viruses is out @sciimmunology.bsky.social This was a herculean effort brilliantly led by @pauljbaker.bsky.social who singlehandedly established the model in the lab during the pandemic. 🧪 #Immunosky 1/9

Pyroptotic cell corpses are crowned with F-actin-rich filopodia that engage CLEC9A signaling in incoming dendritic cells - Nature Immunology Pyroptotic cell death results in inflammation. Here the authors find that F-actin-rich structures formed during macrophage pyroptosis persist after cell death to activate dendritic cells.

#NoTimeToDie! @inflammasomelab, Holley, Monteleone &co show @natimmunol.bsky.social that cells that die by #pyroptosis, or #necroptosis, are crowned with F-actin filopodia that makes them visible by dendritic cells via CLEC9A to initiate adaptive immunity! www.nature.com/articles/s41...

Divergent roles of RIPK3 and MLKL in high-fat diet–induced obesity and MAFLD in mice Cell death frequently occurs in the pathogenesis of obesity and metabolic dysfunction–associated fatty liver disease (MAFLD). However, the exact contribution of core cell death machinery to disease ma...

Hi bluesky, just wanted to share our most recent paper from the
@katelawlorlab.bsky.social showing distinct roles for #necroptosis effectors RIPK3 (+ Caspase-8) that drives inflammation, and MLKL which regulates lipid handling in obesity-induced #MAFLD. www.life-science-alliance.org/content/8/1/...