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DTSTART;VALUE=DATE:20250515
DTEND;VALUE=DATE:20250516
DTSTAMP:20260408T172640
CREATED:20250430T141408Z
LAST-MODIFIED:20250507T135302Z
UID:61660-1747267200-1747353599@www.crct-inserm.fr
SUMMARY:Workshop ARN & Cancer 2025
DESCRIPTION:3ème Workshop ARN & Cancer \nEn savoir +
URL:https://www.crct-inserm.fr/evenement/workshop-arn-cancer-2025/
LOCATION:Amphithéâtre IUCT-O
CATEGORIES:Animation scientifique
ATTACH;FMTTYPE=image/png:https://www.crct-inserm.fr/wp-content/uploads/2025/04/programme-workshop-15.05.25.png
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BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20250521T100000
DTEND;TZID=Europe/Paris:20250521T123000
DTSTAMP:20260408T172640
CREATED:20250430T093803Z
LAST-MODIFIED:20250430T094559Z
UID:61632-1747821600-1747830600@www.crct-inserm.fr
SUMMARY:MINI WORKSHOP | Lighting the fire: inflammasomes and  pyroptosis in cancer and neurodegeneration
DESCRIPTION:Toutes les informations :\n  \n\nAbstract:\nInflammasomes are intracellular multi-protein complexes that play essential functions in immunity against pathogens. Specifically\, inflammasomes both promote a regulated form of cell death termed pyroptosis and trigger the release of the key inflammatory cytokines interleukin (IL)-1β and IL-18\, two important processes in controlling microbial infections. Because of their involvement in various pathophysiological conditions\, our understanding of inflammasomes has generated an ever-growing interest in the scientific and medical communities over the last 20 years. Yet\, most of this knowledge comes either from the use of rodent models\, which may lack the specific structural and functional characteristics of human inflammasomes\, or from the use of immune cells\, which express a wide range of inflammasomes but lack inflammasomes specifically enriched in non-immune cells.\nIn this context\, I will discuss about novel findings on the crucial immune function of the human NLRP1 inflammasome\, highly expressed in airway\, skin and corneal epithelia\, in response to a broad range of infections but also environmental threats that converge to a specific stress pathway\, the ribotoxic stress response. Specifically I will adress our very recent findings that unexpectedely link dna damage and ribotoxic stress-induced nlrp1 inflammasome response upon chemotherapy and microbial genotoxin exposure. \n  \n\nAbstract:\nProkaryotic pore-forming toxins drive inflammasome activation and pyroptosis through K+-dependent activation of the canonical NLRP3/caspase-1/gasdermin D signaling axis. In this study\, we hypothesized that perforin\, a eukaryotic pore-forming protein released into the lytic synapse by antigen-specific cytotoxic T lymphocytes (CTLs) upon cognate antigen recognition\, mimics the pro-pyroptotic activity of ancestral pore-forming toxins\, complementing its role as a conduit for granzymes. Utilizing imaging and molecular approaches\, we demonstrate that perforation of target cells upon CTL attack elicits swift K+ efflux followed by NLRP3-dependent activation of proinflammatory caspase-1 and its major substrate\, the pyroptotic executioner gasdermin D (GSDMD). Acute target cell death upon CTL attack is gasdermin-dependent and demonstrates morphological and molecular features of pyroptosis\, including pyroptotic body formation\, cell bloating\, plasma membrane rupture\, and release of intracellular contents; by contrast\, sustained interaction with CTLs unmasks a delayed apoptotic phenotype in the remaining target cells. Perforation of target cells by soluble perforin is sufficient to trigger rapid K+ efflux\, caspase-1 activation\, and pyroptosis. Our results reveal a novel mechanism for engagement of pyroptotic machinery upon CTL attack\, in which perforin itself can autonomously engage programmed cell death (PCD)\, highlighting the complexity and diversity of the CTL lytic arsenal. \n  \n\nAbstract:\nPyroptosis is a highly inflammatory form of regulated cell death driven by pore-forming gasdermin (GSDM) proteins. Following proteolytic activation\, GSDMs form oligomeric pores that promote plasma membrane rupture (PMR) and amplify the inflammatory response. Canonical pyroptosis is initiated by inflammasome complexes\, which recruit and mature caspase-1 to activate GSDMD. Independently of the inflammasome\, GSDME can transition apoptosis to pyroptosis following cleavage by caspase-3. A subset of HIV[+] patients experience progressive cognitive impairment and neurodegeneration (NeuroHIV) driven by infection of brain myeloid cells. However\, the mechanisms which underlie neuronal injury remain uncertain. We hypothesized that the inflammasome-pyroptosis axis (IPA) in neurons directly mediates HIV-associated neurodegeneration. Examination of primary human neural cultures revealed GSDMD is restricted to glial cells\, whereas neurons selectively express GSDME. Neurons exposed to HIV viral protein R (Vpr)\, an established NLRP3 inflammasome stimulus\, showed substantial neurite retraction and PMR with activation of caspases-1\, -3 and GSDME. Genetic knockdown of NLRP3\, caspase-1\, or GSDME significantly reduced neuronal PMR. Furthermore\, caspase-1 inhibition limited caspase-3/GSDME cleavage and neurite degradation\, suggesting that inflammasome signalling initiates neuronal pyroptosis. Direct activation of caspase-1 using an optogenetic approach verified these findings\, resulting in rapid activation of the caspase-3/GSDME axis\, PMR and cell death morphologically consistent with pyroptosis. Furthermore\, analysis of cortical brain tissues from persons with NeuroHIV and in an associated macaque model (NeuroSIV) revealed GSDME cleavage and markers of neuronal pyroptosis. Our findings demonstrate neuronal IPA signalling with downstream GSDME activation can directly contribute to HIV-associated neurodegeneration. \nPour suivre le mini workshop à distance\, cliquez ici.
URL:https://www.crct-inserm.fr/evenement/mini-workshop-lighting-the-fire-inflammasomes-and-pyroptosis-in-cancer-and-neurodegeneration/
LOCATION:Salle Cazaux + Visio Teams
CATEGORIES:Animation scientifique
ATTACH;FMTTYPE=image/png:https://www.crct-inserm.fr/wp-content/uploads/2025/04/mini-workshop.png
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BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20250523T110000
DTEND;TZID=Europe/Paris:20250523T120000
DTSTAMP:20260408T172640
CREATED:20250429T083834Z
LAST-MODIFIED:20250512T080838Z
UID:61614-1747998000-1748001600@www.crct-inserm.fr
SUMMARY:Conférence | Jean Monlong\, IRSD
DESCRIPTION:Bio:\nJean Monlong has been working with sequencing data for more than 10 years\, first on transcriptomics as a master student in Barcelona at the Centre for Genomic Regulation with Roderic Guigo\, then switching to genomics during his PhD at McGill University in Montreal with Guillaume Bourque. He then joined the University of California\, Santa Cruz for his postdoc to work on variant calling with pangenomes in the group of Benedict Paten. Since 2023\, Jean is a Chargé de Recherche INSERM at the Institut de Recherche en Santé Digestive (IRSD) where he continues using pangenomes and sequencing technologies to improve the analysis of human genomes and the functional interpretation of genomic variation.\n\n\nAbstract:\nVariant affecting more than 50 nucleotides\, or structural variants\, can have important functional impacts. They unfortunately tend to be understudied because of technical challenges hindering their detection. I will present two approaches to integrate those variants in genomic studies. The first uses pangenomes as augmented reference genome containing common variants (including structural variants). With this more complete reference\, short sequencing reads are better analyzed\, resulting in a larger number of structural variants that can be genotyped accurately. The second approach uses cost-efficient long read sequencing technology\, such as Oxford Nanopore\, to infer phased variants at unprecedented resolution.
URL:https://www.crct-inserm.fr/evenement/conference-jean-monlong-irsd/
LOCATION:Salle Cazaux
CATEGORIES:Animation scientifique
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