Cellular and Molecular Gastroenterology and Hepatology最新文献

{"title":"Trailblazing TRAIL Therapy: Illuminating Pathways for Cholangiocarcinoma Treatment","authors":"Sungjin Ko","doi":"10.1016/j.jcmgh.2024.02.008","DOIUrl":"10.1016/j.jcmgh.2024.02.008","url":null,"abstract":"","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":null,"pages":null},"PeriodicalIF":7.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352345X24000365/pdfft?md5=d443e504f6049522c33c4cb83c703f7c&pid=1-s2.0-S2352345X24000365-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140023451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IGF2BP1/IMP1 Deletion Enhances a Facultative Stem Cell State via Regulation of MAP1LC3B","authors":"Louis R. Parham ,&nbsp;Patrick A. Williams ,&nbsp;Kay Katada ,&nbsp;Shaneice K. Nettleford ,&nbsp;Priya Chatterji ,&nbsp;Kofi K. Acheampong ,&nbsp;Charles H. Danan ,&nbsp;Xianghui Ma ,&nbsp;Lauren A. Simon ,&nbsp;Kaitlyn E. Naughton ,&nbsp;Rei Mizuno ,&nbsp;Tatiana Karakasheva ,&nbsp;Emily A. McMillan ,&nbsp;Kelly A. Whelan ,&nbsp;Donita C. Brady ,&nbsp;Sydney M. Shaffer ,&nbsp;Kathryn E. Hamilton","doi":"10.1016/j.jcmgh.2023.12.001","DOIUrl":"10.1016/j.jcmgh.2023.12.001","url":null,"abstract":"<div><h3>Background &amp; Aims</h3><p>The intestinal epithelium interfaces with a diverse milieu of luminal contents while maintaining robust digestive and barrier functions. Facultative intestinal stem cells are cells that survive tissue injury and divide to re-establish the epithelium. Prior studies have shown autophagic state as functional marker of facultative intestinal stem cells, but regulatory mechanisms are not known. The current study evaluated a post-transcriptional regulation of autophagy as an important factor for facultative stem cell state and tissue regeneration.</p></div><div><h3>Methods</h3><p>We evaluated stem cell composition, autophagic vesicle content, organoid formation, and in vivo regeneration in mice with intestinal epithelial deletion of the RNA binding protein <em>IGF2</em> messenger RNA binding protein 1 (IMP1). The contribution of autophagy to resulting in vitro and in vivo phenotypes was evaluated via genetic inactivation of <em>Atg7</em>. Molecular analyses of IMP1 modulation of autophagy at the protein and transcript localization levels were performed using IMP1 mutant studies and single-molecule fluorescent in situ hybridization.</p></div><div><h3>Results</h3><p>Epithelial <em>Imp1</em> deletion reduced leucine rich repeat containing G protein coupled receptor 5 cell frequency but enhanced both organoid formation efficiency and in vivo regeneration after irradiation. We confirmed prior studies showing increased autophagy with IMP1 deletion. Deletion of <em>Atg7</em> reversed the enhanced regeneration observed with <em>Imp1</em> deletion. IMP1 deletion or mutation of IMP1 phosphorylation sites enhanced expression of essential autophagy protein microtubule-associated protein 1 light chain 3β. Furthermore, immunofluorescence imaging coupled with single-molecule fluorescent in situ hybridization showed IMP1 colocalization with <em>MAP1LC3B</em> transcripts at homeostasis. Stress induction led to decreased colocalization.</p></div><div><h3>Conclusions</h3><p>Depletion of IMP1 enhances autophagy, which promotes intestinal regeneration via expansion of facultative intestinal stem cells.</p></div>","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":null,"pages":null},"PeriodicalIF":7.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352345X2300214X/pdfft?md5=a5294ecfdf885b7c2780c0ea378dd133&pid=1-s2.0-S2352345X2300214X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138562828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Recurrent Liver MAN2A1-FER Oncoprotein Lacks Kinase Activity: Implications for the Use of Tyrosine Kinase Inhibitors","authors":"Mathieu Desaunay,&nbsp;Edwige Voisset,&nbsp;Sebastien Letard,&nbsp;Philippe Roche,&nbsp;Paulo De Sepulveda","doi":"10.1016/j.jcmgh.2023.12.007","DOIUrl":"10.1016/j.jcmgh.2023.12.007","url":null,"abstract":"","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":null,"pages":null},"PeriodicalIF":7.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352345X23002205/pdfft?md5=a38de6963a10ccc7458cbedd3fc6acf1&pid=1-s2.0-S2352345X23002205-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139028038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Protein Complex of Liver Origin Activates a Pro-inflammatory Program That Drives Hepatic and Intestinal Injury in Alcohol-Associated Liver Disease","authors":"Xiaodong Ge ,&nbsp;Hui Han ,&nbsp;Romain Desert ,&nbsp;Sukanta Das ,&nbsp;Zhuolun Song ,&nbsp;Sai Santosh Babu Komakula ,&nbsp;Wei Chen ,&nbsp;Dipti Athavale ,&nbsp;Daniel Lantvit ,&nbsp;Natalia Nieto","doi":"10.1016/j.jcmgh.2024.05.010","DOIUrl":"10.1016/j.jcmgh.2024.05.010","url":null,"abstract":"<div><h3>Background &amp; Aims</h3><p>There is limited information on how the liver-to-gut axis contributes to alcohol-associated liver disease (AALD). We previously identified that high-mobility group box-1 (HMGB1) undergoes oxidation in hepatocytes and demonstrated elevated serum levels of oxidized HMGB1 ([O] HMGB1) in alcoholic patients. Since interleukin-1 beta (IL-1B) increases in AALD, we hypothesized hepatocyte-derived [O] HMGB1 could interact with IL-1B to activate a pro-inflammatory program that, besides being detrimental to the liver, drives intestinal barrier dysfunction.</p></div><div><h3>Results</h3><p>Alcohol-fed <em>Rage</em>^ΔMye mice exhibited decreased nuclear factor kappa B signaling, a pro-inflammatory signature, and reduced total intestinal permeability, resulting in protection from AALD. In addition, [O] HMGB1 bound and signaled through the receptor for advanced-glycation end-products (RAGE) in myeloid cells, driving hepatic inflammation, intestinal permeability, and increased portal blood lipopolysaccharide in AALD. We identified that [O] HMGB1 formed a complex with IL-1B, which was found in the livers of patients with acute alcoholic hepatitis and mice with AALD. This complex originated from the liver, because it was absent in the intestine when hepatocytes did not produce [O] HMGB1. Mechanistically, the complex bound RAGE in Kupffer cells and macrophages induced a pro-inflammatory program. Moreover, it bound RAGE in intestinal macrophages and epithelial cells, leading to intestinal inflammation, altered intestinal epithelial cell tight junction protein expression, increased intestinal permeability, and elevated portal blood lipopolysaccharide, enhancing AALD pathogenesis.</p></div><div><h3>Conclusions</h3><p>We identified a protein complex of liver origin that amplifies the pro-inflammatory feedback loop in AALD; therefore, targeting this complex could have significant therapeutic potential.</p></div>","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":null,"pages":null},"PeriodicalIF":7.1,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352345X24001164/pdfft?md5=7d69d746edcf32f0cd528be96ec7279b&pid=1-s2.0-S2352345X24001164-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141094737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic Variation Between Small Bowel and Colon-Predominant Crohn's Disease","authors":"Halee Patel,&nbsp;R. Alan Harris,&nbsp;Justin H. Qian,&nbsp;Numan Oezguen,&nbsp;Ashleigh Watson,&nbsp;Reka G. Szigeti,&nbsp;Stanley Cho,&nbsp;Wenly Ruan,&nbsp;Savini Britto,&nbsp;Antone Opekun,&nbsp;Geoffrey Preidis,&nbsp;Richard Kellermayer","doi":"10.1016/j.jcmgh.2024.02.010","DOIUrl":"10.1016/j.jcmgh.2024.02.010","url":null,"abstract":"","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":null,"pages":null},"PeriodicalIF":7.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352345X24000389/pdfft?md5=47811aecfd1ff6d9066f4683f258cc80&pid=1-s2.0-S2352345X24000389-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139900930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Of Sugar and Fat: How Protein Glycosylation in Sinusoidal Cells Controls Lipid Metabolism in Liver","authors":"Frédéric P. Lemaigre","doi":"10.1016/j.jcmgh.2024.03.010","DOIUrl":"10.1016/j.jcmgh.2024.03.010","url":null,"abstract":"","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":null,"pages":null},"PeriodicalIF":7.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352345X24000626/pdfft?md5=178d449b36e20ab409c6a3ae600c6cbd&pid=1-s2.0-S2352345X24000626-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140793676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interplay Between Drug-Induced Liver Injury and Gut Microbiota: A Comprehensive Overview","authors":"Guolin Li ,&nbsp;Yifu Hou ,&nbsp;Changji Zhang ,&nbsp;Xiaoshi Zhou ,&nbsp;Furong Bao ,&nbsp;Yong Yang ,&nbsp;Lu Chen ,&nbsp;Dongke Yu","doi":"10.1016/j.jcmgh.2024.05.003","DOIUrl":"10.1016/j.jcmgh.2024.05.003","url":null,"abstract":"<div><p>Drug-induced liver injury is a prevalent severe adverse event in clinical settings, leading to increased medical burdens for patients and presenting challenges for the development and commercialization of novel pharmaceuticals. Research has revealed a close association between gut microbiota and drug-induced liver injury in recent years. However, there has yet to be a consensus on the specific mechanism by which gut microbiota is involved in drug-induced liver injury. Gut microbiota may contribute to drug-induced liver injury by increasing intestinal permeability, disrupting intestinal metabolite homeostasis, and promoting inflammation and oxidative stress. Alterations in gut microbiota were found in drug-induced liver injury caused by antibiotics, psychotropic drugs, acetaminophen, antituberculosis drugs, and antithyroid drugs. Specific gut microbiota and their abundance are associated closely with the severity of drug-induced liver injury. Therefore, gut microbiota is expected to be a new target for the treatment of drug-induced liver injury. This review focuses on the association of gut microbiota with common hepatotoxic drugs and the potential mechanisms by which gut microbiota may contribute to the pathogenesis of drug-induced liver injury, providing a more comprehensive reference for the interaction between drug-induced liver injury and gut microbiota.</p></div>","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":null,"pages":null},"PeriodicalIF":7.1,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352345X24001097/pdfft?md5=7d0a80349d59da5cc87143fa65f5ff6b&pid=1-s2.0-S2352345X24001097-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140905214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bacterial Sphingolipids Exacerbate Colitis by Inhibiting ILC3-derived IL-22 Production","authors":"Bin Bao ,&nbsp;Youyuan Wang ,&nbsp;Pavl Boudreau ,&nbsp;Xinyang Song ,&nbsp;Meng Wu ,&nbsp;Xi Chen ,&nbsp;Izabel Patik ,&nbsp;Ying Tang ,&nbsp;Jodie Ouahed ,&nbsp;Amit Ringel ,&nbsp;Jared Barends ,&nbsp;Chuan Wu ,&nbsp;Emily Balskus ,&nbsp;Jay Thiagarajah ,&nbsp;Jian Liu ,&nbsp;Michael R. Wessels ,&nbsp;Wayne Isaac Lencer ,&nbsp;Dennis L. Kasper ,&nbsp;Dingding An ,&nbsp;Bruce Harold Horwitz ,&nbsp;Scott B. Snapper","doi":"10.1016/j.jcmgh.2024.04.007","DOIUrl":"10.1016/j.jcmgh.2024.04.007","url":null,"abstract":"<div><h3>Background &amp; Aims</h3><p>Gut bacterial sphingolipids, primarily produced by Bacteroidetes, have dual roles as bacterial virulence factors and regulators of the host mucosal immune system, including regulatory T cells and invariant natural killer T cells. Patients with inflammatory bowel disease display altered sphingolipids profiles in fecal samples. However, how bacterial sphingolipids modulate mucosal homeostasis and regulate intestinal inflammation remains unclear.</p></div><div><h3>Methods</h3><p>We used dextran sodium sulfate (DSS)-induced colitis in mice monocolonized with <em>Bacteroides fragilis</em> strains expressing or lacking sphingolipids to assess the influence of bacterial sphingolipids on intestinal inflammation using transcriptional, protein, and cellular analyses. Colonic explant and organoid were used to study the function of bacterial sphingolipids. Host mucosal immune cells and cytokines were profiled and characterized using flow cytometry, enzyme-linked immunosorbent assay, and Western blot, and cytokine function in vivo was investigated by monoclonal antibody injection.</p></div><div><h3>Results</h3><p><em>B fragilis</em> sphingolipids exacerbated intestinal inflammation. Mice monocolonized with <em>B fragilis</em> lacking sphingolipids exhibited less severe DSS-induced colitis. This amelioration of colitis was associated with increased production of interleukin (IL)-22 by ILC3. Mice colonized with <em>B fragilis</em> lacking sphingolipids following DSS treatment showed enhanced epithelial STAT3 activity, intestinal cell proliferation, and antimicrobial peptide production. Protection against DSS colitis associated with <em>B fragilis</em> lacking sphingolipids was reversed on IL22 blockade. Furthermore, bacterial sphingolipids restricted epithelial IL18 production following DSS treatment and interfered with IL22 production by a subset of ILC3 cells expressing both IL18R and major histocompatibility complex class II.</p></div><div><h3>Conclusions</h3><p><em>B fragilis</em>–derived sphingolipids exacerbate mucosal inflammation by impeding epithelial IL18 expression and concomitantly suppressing the production of IL22 by ILC3 cells.</p></div>","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":null,"pages":null},"PeriodicalIF":7.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352345X24001048/pdfft?md5=59a34194ef86160c5f3532ad4c9dd497&pid=1-s2.0-S2352345X24001048-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140868804","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enteric Nervous System Striped Patterning and Disease: Unexplored Pathophysiology","authors":"Lori B. Dershowitz ,&nbsp;Julia A. Kaltschmidt","doi":"10.1016/j.jcmgh.2024.03.004","DOIUrl":"10.1016/j.jcmgh.2024.03.004","url":null,"abstract":"<div><p>The enteric nervous system (ENS) controls gastrointestinal (GI) motility, and defects in ENS development underlie pediatric GI motility disorders. In disorders such as Hirschsprung’s disease (HSCR), pediatric intestinal pseudo-obstruction (PIPO), and intestinal neuronal dysplasia type B (INDB), ENS structure is altered with noted decreased neuronal density in HSCR and reports of increased neuronal density in PIPO and INDB. The developmental origin of these structural deficits is not fully understood. Here, we review the current understanding of ENS development and pediatric GI motility disorders incorporating new data on ENS structure. In particular, emerging evidence demonstrates that enteric neurons are patterned into circumferential stripes along the longitudinal axis of the intestine during mouse and human development. This novel understanding of ENS structure proposes new questions about the pathophysiology of pediatric GI motility disorders. If the ENS is organized into stripes, could the observed changes in enteric neuron density in HSCR, PIPO, and INDB represent differences in the distribution of enteric neuronal stripes? We review mechanisms of striped patterning from other biological systems and propose how defects in striped ENS patterning could explain structural deficits observed in pediatric GI motility disorders.</p></div>","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":null,"pages":null},"PeriodicalIF":7.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352345X24000560/pdfft?md5=cf202a674057981018c678e8581f1c1d&pid=1-s2.0-S2352345X24000560-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140121447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Noncanonical TRAIL Signaling Promotes Myeloid-Derived Suppressor Cell Abundance and Tumor Growth in Cholangiocarcinoma","authors":"Emilien J. Loeuillard ,&nbsp;Binbin Li ,&nbsp;Hannah E. Stumpf ,&nbsp;Jingchun Yang ,&nbsp;Jessica R. Willhite ,&nbsp;Jennifer L. Tomlinson ,&nbsp;Fred Rakhshan Rohakhtar ,&nbsp;Vernadette A. Simon ,&nbsp;Rondell P. Graham ,&nbsp;Rory L. Smoot ,&nbsp;Haidong Dong ,&nbsp;Sumera I. Ilyas","doi":"10.1016/j.jcmgh.2024.01.006","DOIUrl":"10.1016/j.jcmgh.2024.01.006","url":null,"abstract":"<div><h3>Background &amp; Aims</h3><p>Proapoptotic tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) signaling as a cause of cancer cell death is a well-established mechanism. However, TRAIL-receptor (TRAIL-R) agonists have had very limited anticancer activity in human beings, challenging the concept of TRAIL as a potent anticancer agent. Herein, we aimed to define mechanisms by which TRAIL⁺ cancer cells can leverage noncanonical TRAIL signaling in myeloid-derived suppressor cells (MDSCs) promoting their abundance in murine cholangiocarcinoma (CCA).</p></div><div><h3>Methods</h3><p>Multiple immunocompetent syngeneic, orthotopic models of CCA were used. Single-cell RNA sequencing and cellular indexing of transcriptomes and epitopes by sequencing of CD45⁺ cells in murine tumors from the different CCA models was conducted.</p></div><div><h3>Results</h3><p>In multiple immunocompetent murine models of CCA, implantation of TRAIL⁺ murine cancer cells into <em>Trail-r</em>^<em>-/-</em> mice resulted in a significant reduction in tumor volumes compared with wild-type mice. Tumor-bearing <em>Trail-r</em>^<em>-/-</em> mice had a significant decrease in the abundance of MDSCs owing to attenuation of MDSC proliferation. Noncanonical TRAIL signaling with consequent nuclear factor-κB activation in MDSCs facilitated enhanced MDSC proliferation. Single-cell RNA sequencing and cellular indexing of transcriptomes and epitopes by sequencing of immune cells from murine tumors showed enrichment of a nuclear factor-κB activation signature in MDSCs. Moreover, MDSCs were resistant to TRAIL-mediated apoptosis owing to enhanced expression of cellular FLICE inhibitory protein, an inhibitor of proapoptotic TRAIL signaling. Accordingly, cellular FLICE inhibitory protein knockdown sensitized murine MDSCs to TRAIL-mediated apoptosis. Finally, cancer cell–restricted deletion of <em>Trail</em> significantly reduced MDSC abundance and murine tumor burden.</p></div><div><h3>Conclusions</h3><p>Our findings highlight the therapeutic potential of targeting TRAIL⁺ cancer cells for treatment of a poorly immunogenic cancer.</p></div>","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":null,"pages":null},"PeriodicalIF":7.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352345X24000055/pdfft?md5=b89f7c56e45a1fe15f09ae8c7aa77e65&pid=1-s2.0-S2352345X24000055-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139466199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}