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netic findings pharmacological activation of tmem175 with small molecule agonists restored lysosomal functions and reduced α synuclein aggregation in tmem175 l275r neurons in in vivo studies equivalent site mutation knock in mice demonstrated synucleinopathy and pd like motor phenotypes collectively our work provides genetic and pharmacological evidence that severe loss of function mutations may contribute causally to the onset age and pathogenesis of pd and identifies lysosomal proton channels and transporters as potential therapeutic targets for pd intervention authors xiaotong yang ping li man lv lingyong wang ruyi shan zikai jiang danzhen chen fangqian huang weijie cai liding zhao zuoyou guo xinhui chen zhidong cen yichang wang wei yang xinran li wei luo lin yang meiqin hu haoxing xu enhancing treg persistence by inhibiting necroptosis restrains autoimmune pathology qiaoyan wu na cui li gao zhihui lu xiang ao rui pang xingyan li heling pan daichao xu peiying li junying yuan chengyu zou qiaoyan wu na cui li gao zhihui lu xiang ao rui pang xingyan li heling pan daichao xu peiying li junying yuan chengyu zou view text pdf enhancing treg persistence by inhibiting necroptosis restrains autoimmune pathology text pdf abstract regulatory t cells tregs hold great promise as next generation therapeutics for autoimmune diseases however maintaining their functional persistence within inflamed tissues remains a major translational challenge using an in vitro system that recapitulates the inflammatory cns milieu of multiple sclerosis ms together with a pooled shrna screen we identify necroptotic signaling as a key driver of treg death thereby compromising treg functional persistence under inflammatory conditions we further demonstrate that tregs in both a mouse model of ms and patients with ms exhibited a preferential susceptibility to receptor interacting serine threonine kinase 1 dependent ripk1 dependent necroptosis mechanistically a foxp3 driven low glucose metabolic program rendered tregs intrinsically susceptible to necroptosis by limiting o glcnacylation o glcnac modification on ripk1 this vulnerability was not shared by conventional t cells under comparable inflammatory conditions finally in combination with adoptive treg transfer we show that selective inhibition of necroptosis in tregs enhanced their survival and suppressive function at sites of active inflammation thereby reducing autoimmune pathology in mouse models of ms and systemic lupus erythematosus together these findings identify necroptotic cell death as a barrier to treg persistence within inflamed tissues and highlight the therapeutic potential of necroptosis resistant tregs for the treatment of autoimmune diseases authors qiaoyan wu na cui li gao zhihui lu xiang ao rui pang xingyan li heling pan daichao xu peiying li junying yuan chengyu zou gene specific machine learning model epipred identifies likely pathogenic variants in the epilepsy related gene stxbp1 jeffrey d calhoun chengbing wang carina g biar jonathan r gunti john s lee aaron m geller jung h hong santiago schnell louis t dang yu wang jack m parent lori l isom michael d uhler heather c mefford m elizabeth ross vanessa aguiar pulido gemma l carvill jeffrey d calhoun chengbing wang carina g biar jonathan r gunti john s lee aaron m geller jung h hong santiago schnell louis t dang yu wang jack m parent lori l isom michael d uhler heather c mefford m elizabeth ross vanessa aguiar pulido gemma l carvill view text pdf gene specific machine learning model epipred identifies likely pathogenic variants in the epilepsy related gene stxbp1 text pdf abstract stxbp1 variants are a frequent cause of early onset developmental and epileptic encephalopathies and related neurodevelopmental disorders but the clinical interpretation of these variants remains a major challenge most reported stxbp1 missense variants are classified as variants of uncertain significance vus complicating diagnosis counseling and patient eligibility for precision therapies here we developed epipred a gene specific machine learning classifier that predicts the pathogenicity of stxbp1 missense variants and tests these predictions using empirical evidence from well established cellular assays trained on a curated set of pathogenic and benign variants epipred outperformed global prediction tools in accuracy sensitivity and specificity we validated the model s predictions using variant effect assays that measure protein abundance solubility stability and interaction with the snare complex partner syntaxin 1 these biochemical readouts aligned closely with model outputs and enabled reclassification of several possibly misdiagnosed variants which warrant further validation and clinical reevaluation we deployed epipred in an interactive web application that allows clinicians researchers and patients to explore predictions for all possible stxbp1 missense variants by identifying likely pathogenic stxbp1 variants including those that may respond to emerging therapies such as protein stabilizers by coupling gene calibrated machine learning with orthogonal variant effect assays and public deployment epipred provides a transferable framework for vus resolution trial enrichment and precision diagnosis across clinically actionable mendelian disease genes authors jeffrey d calhoun chengbing wang carina g biar jonathan r gunti john s lee aaron m geller jung h hong santiago schnell louis t dang yu wang jack m parent lori l isom michael d uhler heather c mefford m elizabeth ross vanessa aguiar pulido gemma l carvill corrigenda corrigendum to markers of compromised gut epithelial barrier integrity increase during the menopause transition albert shieh marta epeldegui arun s karlamangla rheinallt jones roberto pacifici gail a greendale albert shieh marta epeldegui arun s karlamangla rheinallt jones roberto pacifici gail a greendale view text pdf amended article corrigendum to markers of compromised gut epithelial barrier integrity increase during the menopause transition text pdf abstract authors albert shieh marta epeldegui arun s karlamangla rheinallt jones roberto pacifici gail a greendale corrigendum to trem 2 promotes th1 responses by interacting with the cd3ζ zap70 complex following mycobacterium tuberculosis infection yongjian wu minhao wu siqi ming xiaoxia zhan shengfeng hu xingyu li huan yin can cao jiao liu jinai li zhilong wu jie zhou lei liu sitang gong duanman he xi huang yongjian wu minhao wu siqi ming xiaoxia zhan shengfeng hu xingyu li huan yin can cao jiao liu jinai li zhilong wu jie zhou lei liu sitang gong duanman he xi huang view text pdf amended article corrigendum to trem 2 promotes th1 responses by interacting with the cd3ζ zap70 complex following mycobacterium tuberculosis infection text pdf abstract authors yongjian wu minhao wu siqi ming xiaoxia zhan shengfeng hu xingyu li huan yin can cao jiao liu jinai li zhilong wu jie zhou lei liu sitang gong duanman he xi huang corrigendum to slamf7 regulates the inflammatory response in macrophages during polymicrobial sepsis yongjian wu qiaohua wang miao li juanfeng lao huishu tang siqi ming minhao wu sitang gong linhai li lei liu xi huang yongjian wu qiaohua wang miao li juanfeng lao huishu tang siqi ming minhao wu sitang gong linhai li lei liu xi huang view text pdf amended article corrigendum to slamf7 regulates the inflammatory response in macrophages during polymicrobial sepsis text pdf abstract authors yongjian wu qiaohua wang miao li juanfeng lao huishu tang siqi ming minhao wu sitang gong linhai li lei liu xi huang in press preview more cellular senescence mediates facioscapulohumeral muscular dystrophy facioscapulohumeral muscular dystrophy fshd is driven by aberrant expression of the early embryonic transcription factor double homeobox 4 dux4 yet the mechanisms linking low sporadic dux4 research in press preview cell biology muscle biology cellular senescence mediates facioscapulohumeral muscular dystrophy text pdf abstract facioscapulohumeral muscular dystrophy fshd is driven by aberrant expression of the early embryonic transcription factor double homeobox 4 dux4 yet the mechanisms linking low sporadic dux4 activity to progressive muscle degeneration remain unclear here we identify cellular senescence as a central and early mechanism in fshd pathogenesis analysis of patient muscle transcriptomes revealed strong enrichment of senescence and senescence associated secretory phenotype sasp programs that correlated with dux4 activity clinical severity and histopathological changes notably these signatures were detectable even in stir negative muscles defining a prodystrophic state characterized by early molecular alterations preceding overt mri detectable inflammation and highlighting their potential utility as early biomarkers of disease activity using an fshd mouse model we show that dux4 induced muscle injury rapidly triggers senescence which then progressively expands fibroadipogenic progenitors and macrophages emerged as the principal senescent populations and key sources of pro inflammatory and profibrotic sasp signals importantly senescence was therapeutically modifiable treatment with the nucleoside reverse transcriptase inhibitor lamivudine 3tc which inhibits line 1 reverse transcriptase activity significantly reduced senescence inflammation and fibrosis while promoting muscle regeneration these findings identify cellular senescence as a tractable driver of fshd and warrant senotherapeutic strategies particularly lamivudine for clinical intervention in fshd authors usuk jung erdong wei ana mitanoska philipp heher kenric chen haseeb ahsan xu zhang giorgio tasca paul d robbins nathan k lebrasseur michael kyba darko bosnakovski decidua accumulated effector like memory cd8 t cells orchestrate localized antimicrobial defense without compromising fetal tolerance deciphering immune privilege at the maternal fetal interface is essential for understanding how reproductive success and host defense are simultaneously maintained decidualization occurring research in press preview immunology reproductive biology decidua accumulated effector like memory cd8 t cells orchestrate localized antimicrobial defense without compromising fetal tolerance text pdf abstract deciphering immune privilege at the maternal fetal interface is essential for understanding how reproductive success and host defense are simultaneously maintained decidualization occurring within the specialized stromal tissue encapsulating the fetus and placenta shapes local immune adaptation required for healthy pregnancy here we identify a decidua enriched effector like memory cd8 t cell subset marked by cd45ra in humans and cx3cr1 in mice these cells preferentially accumulate in the decidua which harbors a cx3cl1 dominant chemokine niche and disruption of cx3cr1 or uterine cx3cl1 impaired their decidual recruitment and tissue localization human cd45ra and murine cx3cr1 decidual memory cd8 t cells shared conserved transcriptional and functional features including enhanced cytotoxic potential and limited inflammatory cytokine production functionally cx3cl1 mediated cd8 t cell accumulation improved local control of prenatal listeria monocytogenes infection and reduced infection associated fetal loss in contrast fetal antigen specific cd8 t cell accumulation and fetal resorption occurred independently of uterine cx3cl1 together our findings define the maternal fetal interface as an active immunological gatekeeper that compartmentalizing cd8 t cell mediated antimicrobial adaptive immunity through the conserved cx3cl1 cx3cr1 axis supporting pathogen specific defense while preserving fetal tolerance authors lu liu xixi huang tingxuan yin xianyang hu hailin yu guohua zhu chunfang xu jiajia chen jiangyuan du hongyan wang qingyu wu wei zhang feng wang huimei wu meirong du targeted gene therapy alleviates epilepsy and hyperexcitability in models of scn2a deficiency pathogenic scn2a loss of function lof variants can cause severe refractory epilepsy with limited treatment options existing scn2a lof mouse models exhibit few spontaneous seizures limiting the research in press preview cell biology neuroscience targeted gene therapy alleviates epilepsy and hyperexcitability in models of scn2a deficiency text pdf abstract pathogenic scn2a loss of function lof variants can cause severe refractory epilepsy with limited treatment options existing scn2a lof mouse models exhibit few spontaneous seizures limiting the dynamic range needed to assess therapeutic efficacy we therefore generated gene trap scn2a deficient mice on the seizure prone dba 2j background these mice experienced hundreds of spontaneous absence seizures per day characterized by concurrent behavioral arrest and eeg spike wave discharges swds partial restoration of scn2a expression reduced seizure burden electrophysiological analysis revealed impaired action potential waveforms yet increased repetitive firing alongside coordinated downregulation of voltage gated potassium channel genes potentially contributing to hyperexcitability given the broad potassium channel downregulation and prior efficacy of kcna1 gene therapy in refractory seizure models we selected kv1 1 as a potential therapeutic target and used a drug controllable adeno associated virus aav to express human kcna1 we found that this intervention normalized elevated neuronal firing and reduced spontaneous seizure burden in scn2a deficient mice extending these findings to a human cell based platform aav mediated kcna1 expression also reduced neuronal firing in human cortical organoids carrying a scn2a truncating variant identified in patients together these findings provide proof of principle for drug controllable kcna1 gene therapy as a promising treatment avenue for epilepsy related to scn2a lof variants authors zaiyang zhang jingliang zhang xiaoling chen brody a deming shivam kant purba mandal harish kothandaraman phillip j sanmiguel manasi s halurkar akila d abeyaratna morgan j robinson iuliia vitko ronald p gaykema chongli yuan nadia a lanman matthew t tegtmeyer dan wang guangping gao riyi shi edward perez reyes yang yang synthetic immunological niche reveals early immune dysregulation and stratifies therapeutic response in type 1 diabetes in type 1 diabetes t1d disease onset and immunotherapy responses vary widely reflecting heterogeneous stage specific immune dysregulation that remains undefined to investigate this research in press preview autoimmunity immunology synthetic immunological niche reveals early immune dysregulation and stratifies therapeutic response in type 1 diabetes text pdf abstract in type 1 diabetes t1d disease onset and immunotherapy responses vary widely reflecting heterogeneous stage specific immune dysregulation that remains undefined to investigate this heterogeneity we engineered microporous polycaprolactone scaffolds that form synthetic immunological niches ins subcutaneously and capture...