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that links lipid metabolism to cell proliferation stress response and cholesterol homeostasis in liver authors yu deng matthew j niederhuber zhichuan zhu austin j hepperla le yu quentin hahn joshua hartsell tooba rashid piotr a mieczkowski hemant kelkar jeremy m simon yanqiong zhang alessandra livraghi butrico meredith j zeller joseph g c kennedy jazmin f depriest jiong li yan zhang xing qiu h ümit kaniskan jian jin corbin d jones laura e herring douglas h phanstiel xiaojing liu jesse r raab brian d strahl pengda liu b cell depletion improves therapeutic index of combination checkpoint blockade in patients with advanced melanoma kavita m dhodapkar antonio matera alyssa m duffy azmain taz renee julia manalo melinda yushak ragini kudchadkar david h lawson madhav v dhodapkar kavita m dhodapkar antonio matera alyssa m duffy azmain taz renee julia manalo melinda yushak ragini kudchadkar david h lawson madhav v dhodapkar view text pdf clinical research and public health b cell depletion improves therapeutic index of combination checkpoint blockade in patients with advanced melanoma text pdf abstract background combined checkpoint blockade ccb of programmed death 1 pd 1 and cytotoxic t lymphocyte associated protein 4 ctla 4 is highly active in melanoma but limited by significant morbidity from immune related adverse events iraes effective strategies to prevent ccb mediated iraes are lacking methods patients with advanced melanoma were randomly assigned to receive standard of care ipilimumab and nivolumab alone arm a ipi nivo n 7 or with one cycle of rituximab arm b ipi nivo rituximab n 7 results patients receiving ipi nivo rituximab experienced lower rates of greater than grade 3 g3 iraes 14 versus 57 and superior g3 irae free survival compared with those in ipi nivo arm 2 year g3 irae free survival 86 versus 29 p 0 01 without adverse impact on tumor regression or survival g3 hypersensitivity reactions to rituximab 43 in arm b prompted trial closure rituximab depleted pretherapy activated naive b cells linked to autoimmunity and enhanced ccb mediated induction of myeloid inflammation and cxcl13 icos cd4 t cells conclusion b cell depletion favorably modulates ccb mediated immune activation and may reduce irae risk trial registration clinicaltrials gov nct03719131 funding nih ca238471 ar077926 ca289978 and ca290302 authors kavita m dhodapkar antonio matera alyssa m duffy azmain taz renee julia manalo melinda yushak ragini kudchadkar david h lawson madhav v dhodapkar krox20 marks sebaceous gland stem cells and regulates their differentiation to maintain skin oil balance yumeng zhang pernelle pulh michelle f pan yi he juanzhu yan annie li renée m mckay lu q le yumeng zhang pernelle pulh michelle f pan yi he juanzhu yan annie li renée m mckay lu q le view text pdf krox20 marks sebaceous gland stem cells and regulates their differentiation to maintain skin oil balance text pdf abstract oil producing sebaceous glands sgs attached to the upper middle portion of hair follicles are indispensable for maintaining skin hydration and their dysfunction leads to dry skin however the molecular mechanisms underlying regulation of sg stem cells remain largely unknown we identified transcription factor krox20 as a marker of sg stem cells that sustains their stemness throughout sg morphogenesis and homeostasis we developed an inducible mouse model in which ablation of krox20 positive cells causes sg loss and rapidly and robustly induces dry flaky alopecia symptoms following induction this model termed xeroflacia xero xerosis fla flaky cia alopecia provides a tool for studying the biology of dry skin furthermore we found that krox20 directly regulates notch1 transcription to orchestrate the balance between sg stem cell self renewal and differentiation small molecule drug modulation of notch1 signaling to activate or inhibit the pathway enabled us to regulate sg differentiation to maintain skin oil levels providing a proof of principle that other signaling pathways downstream of krox20 could be therapeutic targets for sg related diseases authors yumeng zhang pernelle pulh michelle f pan yi he juanzhu yan annie li renée m mckay lu q le a rare tmem175 mutation drives parkinson s disease pathology by disrupting proton gating and lysosomal acidification 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 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 view text pdf a rare tmem175 mutation drives parkinson s disease pathology by disrupting proton gating and lysosomal acidification text pdf abstract transmembrane protein 175 tmem175 implicated in parkinson s disease pd risk has been variably proposed to function as a background k leak channel or a proton activated proton channel in lysosomes here we identified the rare tmem175 variant p l275r in a patient with early onset pd electrophysiological analyses revealed that tmem175 l275r mutant proteins retain normal lysosomal expression and k leak activity but specifically lose proton and agonist dependent activation gating in skin fibroblasts isolated from the patient with pd harboring the monoallelic p l275r mutation tmem175 l275r and in derived induced pluripotent stem cells and induced dopaminergic neurons lysosomal h flux acidification and degradation were impaired these lysosomal defects were corrected upon genome editing to produce the isogenic wt allele cor but appeared when the mutant allele was introduced onto a wt background l275rmut pathological α synuclein aggregation was facilitated in patient derived l275r and mutation introduced l275rmut neurons consistent with these genetic 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 popu...
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