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Kaiwen Chen

@kaiwenchen-lab.bsky.social

Assistant Professor in NUS Singapore. Cell death, innate immunity and host-pathogen interaction.

4 Posts211 Follower 193 Folgt

Kaiwen Chen @kaiwenchen-lab.bsky.social · last yr.

I am excited to share that Michelle's (Hui Wen) PhD work on microbial subversion of innate immune and cell death pathways is now online! Congrats @michelleyeaphw.bsky.social and all co-authors! 🥳 www.embopress.org/doi/full/10....

A bacterial network of T3SS effectors counteracts host pro-inflammatory responses and cell death to promote infection | The EMBO Journal

imageimageHost cells activate cell death pathways in response to bacterial manipulation of innate immune signalling, but the molecular mechanisms underlying this interplay are not fully understood. Th...

embopress.org

JelenaBezbradicaLab @jelenalab.bsky.social · last yr.

The loss of TBK1, or both TBK1 and the related kinase IKKε, results in uncontrolled cell death–driven inflammation. We show that TBK1/IKKε prevent premature cell death by limiting the activity of multiple death pathways in myeloid cells. www.science.org/doi/10.1126/...

TBK1 and IKKε prevent premature cell death by limiting the activity of both RIPK1 and NLRP3 death pathways

TBK1 and IKKe prevent premature cell death by limiting the activity of multiple death pathways in myeloid cells.

science.org

Kaiwen Chen @kaiwenchen-lab.bsky.social · 2y ago

Thrilled to start 2025 with our latest findings! Yersinia invades macrophage cytosol to activate caspase-11 when caspase-8 or YopJ are inactive. www.cell.com/cell-reports...

Plasticity of cell death pathways ensures GSDMD activation during Yersinia pseudotuberculosis infection

Injection of YopJ by Yersinia pseudotuberculosis triggers RIPK1-dependent caspase-8 and GSDMD activation in murine macrophages; however, how macrophages defend against Yersinia when caspase-8 or YopJ ...

cell.com

Mike Lee @theleelab.bsky.social · 2y ago

We just posted a preprint about a death mechanism that we find truly surprising. When you turn off transcription, cells die (duh!)... but did you know this happens due to loss of Pol II itself, not loss of Pol II activity!?! preprint here and a thread (1/n): www.biorxiv.org/content/10.1... 🧪

Pol II degradation activates cell death independently from the loss of transcription

Pol II-mediated transcription is essential for eukaryotic life. While loss of transcription is thought to be universally lethal, the associated mechanisms promoting cell death are not yet known. Here,...

biorxiv.org

Kat Mayer-Barber,PhD @mayerbarber.bsky.social · 2y ago

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

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.

Inflammasome Lab @inflammasomelab.bsky.social · 2y ago

Have you ever wondered whether pyroptotic corpses have functions beyond the grave? We made the surprising discovery that pyroptotic corpses are flagged by #filopodia to alert #DendriticCells they need autopsy. A short Bluetorial (1/13)👇with movies! Link: rdcu.be/d2mjm

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...

rdcu.be

Ivan Zanoni @lozanzi.bsky.social · 2y ago

#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...

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.

nature.com

Jacki Heraud-Farlow @jackiheraudfarlow.bsky.social · 2y ago

Thrilled to share our new paper out today in #ScienceImmunology! It’s been a long time coming and I’m so excited to be able to share it. Skeetorial (is that what we call it here?) to come when it is (a) not Saturday and (b) not my birthday. Best present ever! #ImmunoSky #RNASky

GGNBP2 regulates MDA5 sensing triggered by self double-stranded RNA following loss of ADAR1 editing

GGNBP2, CNOT10, and CNOT11 are required for innate immune response after the loss of ADAR1-mediated editing of self dsRNA.

science.org