Poltorak Lab
@LabPoltorak
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Twitter for Alexander Poltorak's Lab at Tufts University School of Medicine
Joined October 2019
#WeekendRead! #NoTimeToDie! Welcome to a new form of cell death: #efferoptosis! Poltorak, Muendlein &co show @SciImmunology that during systemic inflammation TNF reprograms efferocytic macrophages to activate caspase-8 (not NLRP3!) pyrotosis & IL1b release
science.org
Activation of macrophages engulfing neutrophils by TNF switches efferocytosis to caspase-8–mediated pyroptosis and IL-1β production.
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Activation of macrophages engulfing neutrophils by TNF switches efferocytosis to caspase-8–mediated pyroptosis and IL-1β production @SciImmunology @LabPoltorak
https://t.co/gSsLLw9TAD
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Scientists have found that tumor necrosis factor can switch macrophage #efferocytosis from immunologically silent to pro-inflammatory during #sepsis and systemic inflammation. @LabPoltorak Learn more in Science #Immunology: https://t.co/XmgFOanSCJ
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Excited to have contributed to this paper!!! Read here how STING regulates microglia in aging. Congrats to @kate_sulka and the whole team!!! @CellReports
https://t.co/qe7jmoaDl3
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Have you seen our papers on T-cell Myd88 in HF and cancer (links in 🧵) and wondered what the mechanism at the TCR was? We now outline a novel molecular role for MyD88 acting downstream of the TCR and regulating activation / cell death, out in @J_Immunol
https://t.co/bWHUzFn1L1
academic.oup.com
Abstract. The life cycle of effector T cells is determined by signals downstream of the T cell receptor (TCR) that induce activation and proinflammatory ac
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Thank you to @LabPoltorak @ZoieMagri @PilarAlcaidePhD for making this study possible. Previous papers on T-Myd88 at @CircRes ( https://t.co/IOi2dsj5X3) and @AJPathology ( https://t.co/CaaoFMOQcZ)
ahajournals.org
BACKGROUND: Cardiac inflammation in heart failure is characterized by the presence of damage-associated molecular patterns, myeloid cells, and T cells. Cardiac damage-associated molecular patterns...
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After reporting a role for T cell MyD88 during cardiac adaptation to stress @CircRes & in melanoma @AJPathology, we now decipher a molecular mechanism👇. Thank U @J_Immunol @AbeBayer @LabPoltorak @ZoieMagri @TuftsMedSchool
https://t.co/CGUn7gmQO7
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#EveryCellIsAnImmuneCell!💥Thrilled💥for our new paper @CellCellPress with @achillebro! We show that, during #IBD, type III #interferons delay gut repair by inducing #pyroptosis in intestinal epithelial cells via #gasdermin C upon ZBP1 activation! 1/n
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An exciting Halloween week for the Poltorak lab! Two successful PhD defenses in one week! Congrats David Jetton and @ZoieMagri ! Big thank you to outside examiners @MichelleKellih3 and @Lo_Zanzi for fabulous discussions! @TuftsGSBS
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We found CD14 can switch Fas signaling from pro-death to pro-inflammatory! Check out our recent work in @CellReports to learn more. Congrats to first author @ZoieMagri! https://t.co/uo0J6Tk1qg
cell.com
Activation of the Fas receptor can be pro-death or pro-inflammatory, but little is known about the switch between outcomes. Magri et al. demonstrate that TLR adaptor CD14 can mediate this switch...
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How does RIPK1 drive activation of caspase 8 in Yersinia infection?? Read our latest paper in @CellReports to find out! Congrats to first author David Jetton @TuftsGSBS
https://t.co/kxiGI6et5w
cell.com
The role of specific autophosphorylations driving RIPK1-dependent death is unclear. Jetton et al. demonstrate that autophosphorylation of RIPK1 T169 is required to initiate caspase-8-dependent...
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Neurons repurpose death complex components to induce an anti-viral response during Zika virus infection. In her first preLight, @ZoieMagri covers recent work from the lab of @AndrewOberst. #preprint
#preLight 👉 https://t.co/NJoXro06aW
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A recent preprint from the lab of @AndrewOberst demonstrates that neurons can repurpose death complex components to induce an anti-viral response to Zika! I’ve highlighted their work in my latest preLights post. Check it out! https://t.co/V3pvvVtMXA
prelights.biologists.com
Neurons repurpose death complex components to induce an anti-viral response during Zika virus infection.
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This symposium on #celldeath and survival will discuss exciting developments in this field including inflamed tissues and non-canonical #molecularpathways. Register for #Pathobiology2024 to attend this session! https://t.co/03awtFtBf0
@Penn @TuftsUniversity @NotreDame @YaleMed
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Cell death is essential to your health − an immunologist explains when cells decide to die with a bang or take their quiet leave
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Check out this piece by one of our PhD students @ZoieMagri in the @ConversationUS ! Cell death is essential to your health − an immunologist explains when cells decide to die with a bang or take their quiet leave
theconversation.com
Your cells die to keep you alive. Cell death does everything from fighting cancer cells and pathogens to forming your fingers and toes.
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➡️Join us at the next BCDI meeting on Monday Oct 2nd at 3PM on the Harvard Med Quad (Goldenson 122) for exciting discussions with @chendi on inducing apoptosis in NSCLC and @nabel on identifying novel therapy targets in thymic epithelial tumors. More info: https://t.co/uOJiL13B18
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Intriguingly, & consistent with the earlier work of @LabPoltorak ( https://t.co/SXWdMWJ1kU), Jenna found that unlike in mouse macrophages, WT Yersinia fails to induce cell death in human IECs & macrophages, indicating that human cells are unable to undergo YopJ-mediated death. 4/n
pnas.org
Cell death and inflammation are intimately linked during Yersinia infection. Pathogenic Yersinia inhibits the MAP kinase TGFβ-activated kinase 1 (T...
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