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s 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 tissue associated systemic immune changes building on our prior demonstration of in based longitudinal t1d monitoring we use multimodal in profiling to define the immune changes underlying divergent disease trajectories and immunotherapy responses in non obese diabetic nod mice longitudinal transcriptomic profiling of in identified early myeloid associated changes followed by increasing t cell associated dysregulation that distinguished progressors from non progressors an early stage in based t1d gene signature stratified nod progressors from non progressors by 6 weeks of age and was conserved across human t1d tissues distinguishing t1d from non diabetic individuals in spleen and pancreatic lymph node samples but not in peripheral blood signature based stratification revealed macrophage associated tnfα pathway enrichment in pancreas of nod progressors which was validated in human t1d islets given the heterogeneous response to anti tnfα therapy in profiling identified genesets associated with anti tnfα efficacy and generated a response score that prospectively distinguished treatment sensitive from resistant mice these findings establish in as a platform for detecting stage wise immune dysregulation and stratifying immunotherapy response in t1d authors jyotirmoy roy yifei jiang runbo mao jessica l king amod talekar donglin liu lillian holman haoxuan zeng xin luo laila m rad peter sajjakulnukit brianna ha kai liu elizabeth j bealer bryan wonski kathryn kang sean t carey luke f bugada brooke m smiley shahzad sohail antonio d holmes dominik awad aaron h morris costas a lyssiotis jie liu lonnie d shea biological sex dependent hormonal signaling and metabolomic profiles in obesity alter tumor microenvironment and immunotherapy outcomes commonly viewed as a negative prognostic factor in cancer obesity is associated with improved responses to cancer immunotherapy using immune checkpoint inhibitors icis although data suggest a research in press preview immunology oncology biological sex dependent hormonal signaling and metabolomic profiles in obesity alter tumor microenvironment and immunotherapy outcomes text pdf abstract commonly viewed as a negative prognostic factor in cancer obesity is associated with improved responses to cancer immunotherapy using immune checkpoint inhibitors icis although data suggest a sexual dimorphism influencing the effects of obesity on immunotherapy responses to our knowledge the intersection of sex and obesity on immunotherapy requires further exploration we demonstrate in a pan cancer analysis stratified by sex and bmi that obesity bmi 30 is associated with improved survival after ici only in male patients in preclinical models of diet induced obesity dio we observed that only dio male tumor bearing mice responded better to ici the differential effect of sex on outcomes was associated with alterations in the tumor microenvironment where dio female mice demonstrated increased tumor associated macrophages skewed toward a m2 phenotype ovariectomy of dio female mice reduced m2 polarization and increased anti tumor immune responses including increases in tumor infiltrating t cells following ici metabolomic analysis of dio mice demonstrated distinct profiles base on sex re stratification of female cancer patients revealed that obesity was associated with improved outcome but only in post menopausal age 55 patients we identify that the immunotherapy obesity paradox is sex dependent and that hormonal and metabolomic status modulates the influence of obesity on icis authors logan v vick spencer r rosario ziming wang craig collins lam t khuat yatian yang michael k sheng wahed a firoz ryan n nielsen yao hui sun aryana m razmara hossein borghaei emmanuel s antonarakis andrew elliott nishant gandhi raid aljumaily sami ibrahimi michael machiorlatti sara k vesely shuchi gulati sarbajit mukherjee robert j canter sean j judge arta m monjazeb william j murphy view more articles by topic aging aids hiv angiogenesis autoimmunity bone biology cardiology cell biology clinical research dermatology development endocrinology gastroenterology genetics hematology hepatology immunology infectious disease inflammation metabolism microbiology muscle biology nephrology neuroscience oncology ophthalmology otology public health pulmonology 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