Cell metabolismPub Date : 2026-10-28DOI: 10.1016/j.cmet.2026.10.001
Taisuke Kondo, Makoto Ando, Josquin Moraly, Justyn DuSold, Abdallah Abdelmaksoud, Hannah W Song, Lakshmi Balagopalan, Dongya Jia, Laetitia Racine, Andy D Tran, Sooraj Achar, Serifat O Adebola, Pedro Gonzalez-Menendez, John Buckley, Anjali Chandroth, Alka Dwivedi, Nikolaos Svoronos, Angela Su, Christopher D Chien, Alexander D Clark, Xiyuan Zhang, Bonnie Yates, King Chan, Stephen D Fox, Xia Xu, Nicholas P Restifo, Neeraja Syed, Michael C Kelly, Michael Kruhlak, Yuki Kagoya, Rémy Bosselut, Jack F Shern, Thorkell Andresson, Valérie Dardalhon, Craig J Thomas, Steven L Highfill, Nirali N Shah, Grégoire Altan-Bonnet, Naomi Taylor
{"title":"Arginine rewires eIF4F translation initiation to overcome fever-induced CAR T cell dysfunction.","authors":"Taisuke Kondo, Makoto Ando, Josquin Moraly, Justyn DuSold, Abdallah Abdelmaksoud, Hannah W Song, Lakshmi Balagopalan, Dongya Jia, Laetitia Racine, Andy D Tran, Sooraj Achar, Serifat O Adebola, Pedro Gonzalez-Menendez, John Buckley, Anjali Chandroth, Alka Dwivedi, Nikolaos Svoronos, Angela Su, Christopher D Chien, Alexander D Clark, Xiyuan Zhang, Bonnie Yates, King Chan, Stephen D Fox, Xia Xu, Nicholas P Restifo, Neeraja Syed, Michael C Kelly, Michael Kruhlak, Yuki Kagoya, Rémy Bosselut, Jack F Shern, Thorkell Andresson, Valérie Dardalhon, Craig J Thomas, Steven L Highfill, Nirali N Shah, Grégoire Altan-Bonnet, Naomi Taylor","doi":"10.1016/j.cmet.2026.10.001","DOIUrl":"https://doi.org/10.1016/j.cmet.2026.10.001","url":null,"abstract":"<p><p>Chimeric antigen receptor (CAR) T cell therapy has revolutionized treatment of hematological malignancies, but cytokine release syndrome (CRS) remains a major toxicity. Fever-a hallmark of CRS-has been understudied as a modifier of therapeutic efficacy. In a retrospective cohort of patients with B cell acute lymphoblastic leukemia treated with CD22-directed CAR T cells (NCT02315612), sustained high-grade fever inversely correlated with clinical response. Mechanistically, experimental hyperthermia impaired proximal CAR signaling, reduced cytotoxicity, and compromised metabolic fitness through dysregulated arginine metabolism. Arginine supplementation restored CAR T cell function following hyperthermic stress and enhanced cytotoxicity under normothermic conditions. This effect required mTOR-dependent recruitment of the eIF4F translation-initiation complex and downstream c-MYC-driven metabolic reprogramming. Importantly, arginine enhanced good manufacturing practice (GMP)-manufactured CAR T cell function under normothermia, while oral supplementation improved in vivo efficacy. These findings identify metabolic control of translation as a fever-sensitive checkpoint and establish arginine supplementation as a tractable strategy to enhance CAR T cell efficacy.</p>","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":" ","pages":""},"PeriodicalIF":30.9,"publicationDate":"2026-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149290691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Dynamic force sensing by bone delays aging and extends lifespan.","authors":"Zhimin Zhang, Zhiqing Cai, Shencai Liu, Yun Chu, Zhengtao Jiang, Wuju Zhang, Yating Pan, Ying Lin, Xiaocui Wei, Jingting Chen, Junnan Huangfu, Bocheng Nan, Yibo Zhou, Le Hu, Wenquan Liang, Zhipeng Zou, Minjun Huang, Sheng Lu, Di Lu, Xiaochun Bai","doi":"10.1016/j.cmet.2026.09.020","DOIUrl":"https://doi.org/10.1016/j.cmet.2026.09.020","url":null,"abstract":"<p><p>Physical activity promotes health primarily by decelerating the aging process. Bone is one of the tissues capable of sensing mechanical force and can adapt to different physical demands. However, its role in whole-body aging is unknown. We found that reduced mechano-sensing in osteocytes, caused by deletion of the mechanosensory channel, Piezo1, accelerated whole-body aging in mice. Dynamic tibial axial loading (DTAL) in mice at 20-24 months of age extended both healthspan and lifespan (9.4%/79.5 days). Furthermore, DTAL reversed bone marrow immunosenescence and induced anti-aging and protective factors while downregulating pro-aging and pro-inflammatory factors. We also identified pigment epithelium-derived factor (PEDF) as a novel mechano-responsive anti-aging factor that is highly associated with healthy aging in humans. Thus, our findings highlighted an essential role for bone mechano-sensing in whole-body aging. This could potentially be manipulated to prevent aging, extend health, and aid those unable to exercise or with decreased mobility.</p>","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":" ","pages":""},"PeriodicalIF":30.9,"publicationDate":"2026-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149247744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell metabolismPub Date : 2026-10-08DOI: 10.1016/j.cmet.2026.09.021
Zhiguang Zhou, Zhifeng Cheng, Ping Jin, Guoping Yang, Haifang Wang, Bimin Shi, Qijuan Dong, Xiaoxia Shi, Xiaoguang Shi, Hongyan Shu, Wenli Sun, Chongbing Huang, Shuping Zhao, Li Mao, Wei Wang, Ping Xiong, Xiaowen Chen, Junhang Tian, Haiyan Zhang, Tao Su, Liang Huang, Sofie Bay Simony, Thomas Holst-Hansen, Huiru Yan
{"title":"UBT251, a novel triple GLP-1, GIP, and glucagon receptor agonist, in adults with overweight or obesity: A multicenter, randomized phase 2 trial.","authors":"Zhiguang Zhou, Zhifeng Cheng, Ping Jin, Guoping Yang, Haifang Wang, Bimin Shi, Qijuan Dong, Xiaoxia Shi, Xiaoguang Shi, Hongyan Shu, Wenli Sun, Chongbing Huang, Shuping Zhao, Li Mao, Wei Wang, Ping Xiong, Xiaowen Chen, Junhang Tian, Haiyan Zhang, Tao Su, Liang Huang, Sofie Bay Simony, Thomas Holst-Hansen, Huiru Yan","doi":"10.1016/j.cmet.2026.09.021","DOIUrl":"10.1016/j.cmet.2026.09.021","url":null,"abstract":"<p><p>UBT251 is a novel triple agonist targeting glucagon-like peptide-1, glucose-dependent insulinotropic polypeptide, and glucagon receptors. In this multicenter, randomized, double-blind, placebo-controlled phase 2 trial, 205 adults with overweight or obesity (59.0% women; aged 18-61 years; without type 2 diabetes) received once-weekly UBT251 at 2 mg, 4 mg (initial dose 0.5 mg or 1 mg), or 6 mg, or placebo for 24 weeks. For the primary efficacy endpoint, least-squares mean percentage changes in body weight at week 24 were -19.7% to -13.6% with UBT251 vs. -2.0% with placebo; placebo-adjusted differences were -17.7% (95% confidence interval [CI], -20.8% to -14.6%) to -11.5% (95% CI, -14.1% to -9.0%; all p < 0.001). UBT251 improved waist circumference, body mass index, blood pressure, lipid profiles, and glycemic parameters. The most frequent adverse events were mild-to-moderate gastrointestinal symptoms. UBT251 produced weight reduction with cardiometabolic improvements and an acceptable safety profile, supporting phase 3 evaluation. This study was registered at China Drug Trials Registry (CTR20250288) and ClinicalTrials.gov (NCT07177469).</p>","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":" ","pages":""},"PeriodicalIF":30.9,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149129563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell metabolismPub Date : 2026-10-06Epub Date: 2026-08-10DOI: 10.1016/j.cmet.2026.07.008
Dongdong Wang, Maria Joy Therese Jabile, Fiorella Di Pastena, Logan K Townsend, Elham Ahmadi, Annabelle Hoegl, Alice Payne, Declan C T Lavoie, Battsetseg Batchuluun, Jaya Gautam, Marisa R Morrow, James S V Lally, Rune E Kuhre, Sebastian B Jørgensen, Gregory R Steinberg
{"title":"GDF15 suppresses liver inflammation independently of weight loss through neuroendocrine glucocorticoid signaling.","authors":"Dongdong Wang, Maria Joy Therese Jabile, Fiorella Di Pastena, Logan K Townsend, Elham Ahmadi, Annabelle Hoegl, Alice Payne, Declan C T Lavoie, Battsetseg Batchuluun, Jaya Gautam, Marisa R Morrow, James S V Lally, Rune E Kuhre, Sebastian B Jørgensen, Gregory R Steinberg","doi":"10.1016/j.cmet.2026.07.008","DOIUrl":"10.1016/j.cmet.2026.07.008","url":null,"abstract":"<p><p>Growth differentiation factor 15 (GDF15) is strongly associated with metabolic dysfunction-associated steatohepatitis (MASH), yet whether it promotes or protects against liver injury remains unclear. Using thermoneutral mouse models that closely resemble human MASH, genetic deletion of GDF15 or its receptor GFRAL selectively worsened hepatic inflammation and fibrosis without altering steatosis or insulin resistance. Conversely, recombinant GDF15 reduced liver inflammation and fibrosis more effectively than matched caloric restriction despite identical reductions in food intake, body weight, and steatosis, demonstrating weight-loss-independent hepatoprotection. These effects required GFRAL but were independent of β-adrenergic signaling. Instead, GDF15 activated the hypothalamic-pituitary-adrenal (HPA) axis, increasing circulating corticosterone and hepatic glucocorticoid receptor signaling. Spatial transcriptomics and RNA sequencing demonstrated that GDF15 remodeled the hepatic immune-fibrotic niche by suppressing inflammatory macrophages, plasma B cells, and activated stellate cells while promoting pro-resolving immune programs. Together, these findings identify a GDF15-GFRAL-HPA axis that restrains liver inflammation independently of weight loss.</p>","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":" ","pages":"2128-2142.e6"},"PeriodicalIF":30.9,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148708923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell metabolismPub Date : 2026-10-06Epub Date: 2026-06-29DOI: 10.1016/j.cmet.2026.06.004
Hagit Shapiro, Birgit Jickeli, Idan Niv, Ben Ernan, Eran Elinav
{"title":"The interplay between the microbiome and immune cells in metabolic homeostasis and disease.","authors":"Hagit Shapiro, Birgit Jickeli, Idan Niv, Ben Ernan, Eran Elinav","doi":"10.1016/j.cmet.2026.06.004","DOIUrl":"10.1016/j.cmet.2026.06.004","url":null,"abstract":"<p><p>Microbiome-derived metabolites, including short-chain fatty acids, bile acids, indoles, and lipopolysaccharides, among other bioactives, modulate mammalian immune cells through a variety of molecular processes, including epigenetic remodeling, mitochondrial metabolic reprogramming, and regulation of mTOR and AMPK signaling pathways. These diverse signals shape inflammatory programs that influence metabolic outcomes in a context-dependent manner, which may sustain metabolic health or drive chronic inflammation impacting obesity, type 2 diabetes, metabolic dysfunction-associated steatotic liver disease, and cardiovascular diseases. Here, we review these metabolite-driven immune-metabolic influences and highlight innovative directions in their exploration, including integration of spatial and single-cell multi-omics to deconvolute microbiome-derived signaling networks within metabolic tissues. We further outline emerging microbiome-based therapeutic strategies targeting immune pathways in cardiometabolic disease, ranging from personalized nutrition, precision probiotics, and microbial consortium transplantation to metabolite-based postbiotics. Collectively, advancing our understanding of host immune-microbiome-metabolic interactions may support the development of targeted interventions for the prevention and treatment of cardiometabolic diseases.</p>","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":" ","pages":"1985-2005"},"PeriodicalIF":30.9,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148354979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell metabolismPub Date : 2026-10-06Epub Date: 2026-08-25DOI: 10.1016/j.cmet.2026.07.027
Bao Tran Vuong, Chloé M Delépine, Jacqueline M Ratter-Rieck, Elisabetta Rinaldi, Jean-Baptiste Julla, Emma Cussenot, Marc Diedisheim, Violeta Raverdy, Elise Liu, Justus S Fischer, Matthias Hepprich, Fawaz Alzaid, Camille Blériot, Etienne Becht, Clémence Cornuot, Joe de Keizer, Macine-Bachir Abdelouahab, Magali Chiral, Rebecca Pfeil, Polina Lipaeva, Daniel Dörr, Oana P Zaharia, Théo Jolivet, Julie Alberge, Charline Potier, Kennan Khider, Frédérik Oger, Jean-Pierre Riveline, Tiphaine Vidal-Trecan, Florence Tubach, Candice Estellat, Judith Abecassis, Aymeric Silvin, Samy Hadjadj, Gael Varoquaux, Robert Wagner, Philippe Froguel, Amélie Bonnefond, Pierre-Jean Saulnier, François Pattou, Florent Ginhoux, Michael Roden, Maddalena Trombetta, Louis Potier, Christian Herder, Jean-François Gautier, Marc Y Donath, Riccardo C Bonadonna, Nicolas Venteclef
{"title":"Immunometabolic endotypes define distinct clinical trajectories in type 2 diabetes.","authors":"Bao Tran Vuong, Chloé M Delépine, Jacqueline M Ratter-Rieck, Elisabetta Rinaldi, Jean-Baptiste Julla, Emma Cussenot, Marc Diedisheim, Violeta Raverdy, Elise Liu, Justus S Fischer, Matthias Hepprich, Fawaz Alzaid, Camille Blériot, Etienne Becht, Clémence Cornuot, Joe de Keizer, Macine-Bachir Abdelouahab, Magali Chiral, Rebecca Pfeil, Polina Lipaeva, Daniel Dörr, Oana P Zaharia, Théo Jolivet, Julie Alberge, Charline Potier, Kennan Khider, Frédérik Oger, Jean-Pierre Riveline, Tiphaine Vidal-Trecan, Florence Tubach, Candice Estellat, Judith Abecassis, Aymeric Silvin, Samy Hadjadj, Gael Varoquaux, Robert Wagner, Philippe Froguel, Amélie Bonnefond, Pierre-Jean Saulnier, François Pattou, Florent Ginhoux, Michael Roden, Maddalena Trombetta, Louis Potier, Christian Herder, Jean-François Gautier, Marc Y Donath, Riccardo C Bonadonna, Nicolas Venteclef","doi":"10.1016/j.cmet.2026.07.027","DOIUrl":"10.1016/j.cmet.2026.07.027","url":null,"abstract":"<p><p>Type 2 diabetes (T2D) is a heterogeneous disease, yet current classifications do not capture its clinico-biological complexity or support precision-based care. We developed an endotyping strategy based on routine blood immune cell counts across more than 1,500 individuals with newly diagnosed T2D from three European cohorts. Unsupervised clustering identified four reproducible immune endotypes: severe inflammatory diabetes (SIND), mild inflammatory diabetes (MIND), lymphocyte-rich diabetes (LYRD), and lymphocyte-deficient diabetes (LYDD). Endotypes were stable, robust to de novo clustering, and independent of age, sex, BMI, and HbA1c. SIND and LYDD were associated with increased cardiovascular, renal, and mortality risk across cohorts. Immune endotyping improved cardiovascular risk prediction beyond SCORE2-Diabetes. Multi-omic profiling revealed immunopathological states, with high-risk endotypes characterized by monocyte-driven inflammation and dysregulated lymphocyte programs. The inflammatory profile of SIND was attenuated by IL-1β antagonism and bariatric surgery. These findings establish immune endotyping as a scalable framework for immunometabolic risk stratification in T2D.</p>","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":" ","pages":"2018-2035.e6"},"PeriodicalIF":30.9,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148820515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell metabolismPub Date : 2026-10-06Epub Date: 2026-08-28DOI: 10.1016/j.cmet.2026.08.003
Yong Tang, Ziqing Chen, Hirak Sarkar, Yong Wei, Sereno L Lopez-Darwin, Asael Roichman, Ji Woo Park, Qinglan Li, Cao Fang, Zihong Chen, James Gow, Minhong Shen, Jennifer Shi, Lifei Jiang, Richard Klar, Xiang Hang, Janette R Lugo, Christina J DeCoste, Jennifer M Miller, Wei Wang, Peter Romanienko, Alana L Welm, Ileana M Cristea, Liling Wan, Joshua D Rabinowitz, Yibin Kang
{"title":"Host metadherin coordinates hepatic lipid metabolism and CD8<sup>+</sup> T cell immunity to promote tumor progression.","authors":"Yong Tang, Ziqing Chen, Hirak Sarkar, Yong Wei, Sereno L Lopez-Darwin, Asael Roichman, Ji Woo Park, Qinglan Li, Cao Fang, Zihong Chen, James Gow, Minhong Shen, Jennifer Shi, Lifei Jiang, Richard Klar, Xiang Hang, Janette R Lugo, Christina J DeCoste, Jennifer M Miller, Wei Wang, Peter Romanienko, Alana L Welm, Ileana M Cristea, Liling Wan, Joshua D Rabinowitz, Yibin Kang","doi":"10.1016/j.cmet.2026.08.003","DOIUrl":"10.1016/j.cmet.2026.08.003","url":null,"abstract":"<p><p>Cancer progression is systemically influenced by distant organ dysfunction induced by primary tumors, yet how long-distance tumor-organ crosstalk regulates antitumor immunity remains unclear. Here, we identify host metadherin (MTDH) as a critical regulator of tumor-induced immunosuppression and metabolic reprogramming via tumor-liver interactions. Using Mtdh knockout mouse models, we show that concurrent MTDH loss in hepatocytes and CD8<sup>+</sup> T cells enhances effector T cell function and suppresses tumor growth and metastasis. Mechanistically, tumor-derived extracellular vesicles and particles (EVPs) activate Kupffer cells to secrete tumor necrosis factor α (TNF-α) and TGF-β, which suppress hepatic PPARα-mediated lipid oxidation via nuclear factor κB (NF-κB) signaling. MTDH loss restores hepatic lipid catabolism, reduces systemic lipid levels, and promotes mitochondrial metabolic reprogramming in CD8<sup>+</sup> T cells under lipid-reduced conditions, thereby boosting antitumor immunity. Genetic or pharmacological targeting of MTDH synergizes with anti-PD-1 therapy. These findings establish host MTDH as a key mediator of tumor-liver crosstalk through metabolic and immune interactions, driving systemic cancer progression.</p>","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":" ","pages":"2072-2089.e13"},"PeriodicalIF":30.9,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13623212/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148852064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell metabolismPub Date : 2026-09-01DOI: 10.1016/j.cmet.2026.06.015
Jesse R Poganik, Alibek Moldakozhayev, Jamie N Justice, Matt Kaeberlein, Peter D Adams, Kenneth Rockwood, Luigi Ferrucci, Vadim N Gladyshev
{"title":"Aging vs. biological age: Conceptual considerations for age reversal claims.","authors":"Jesse R Poganik, Alibek Moldakozhayev, Jamie N Justice, Matt Kaeberlein, Peter D Adams, Kenneth Rockwood, Luigi Ferrucci, Vadim N Gladyshev","doi":"10.1016/j.cmet.2026.06.015","DOIUrl":"10.1016/j.cmet.2026.06.015","url":null,"abstract":"<p><p>Whether reversal of biological age and/or aging is possible is among the most actively debated topics in the field of aging. Here, we consider the meaning of biological age reversal and its burden of proof, focusing on foundational issues and the language we use to debate these questions.</p>","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":"38 9","pages":"1746-1750"},"PeriodicalIF":30.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148877007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell metabolismPub Date : 2026-09-01DOI: 10.1016/j.cmet.2026.08.007
Jaeden S Pyburn, Juan Zhao, Ling Wang, Madison B Schank, Addison C Hill, Puja Banik, Holly K Orfield, Culton R Hensley, Adam B Moorman, Yuezu Wu, Mohammad J Hajipour, Shunbin Ning, Mohamed El Gazzar, Jonathan P Moorman, Zhi Q Yao
{"title":"Extending concerns about GLP-1R antibody specificity to human immune cells.","authors":"Jaeden S Pyburn, Juan Zhao, Ling Wang, Madison B Schank, Addison C Hill, Puja Banik, Holly K Orfield, Culton R Hensley, Adam B Moorman, Yuezu Wu, Mohammad J Hajipour, Shunbin Ning, Mohamed El Gazzar, Jonathan P Moorman, Zhi Q Yao","doi":"10.1016/j.cmet.2026.08.007","DOIUrl":"https://doi.org/10.1016/j.cmet.2026.08.007","url":null,"abstract":"","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":"38 9","pages":"1733-1734"},"PeriodicalIF":30.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148877029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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