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deletion of the immunoglobulin heavy chain 3′ regulatory region super-enhancer affects somatic hypermutation in B1 B cells

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Cellular & Molecular Immunology 2019年第2期16卷 195-197页

作者： Issaoui Hussein Ghazzaui Nour Boyer François denizot Yves Saintamand Alexis Centre national de la recherche Scientifique unitéMixte de recherche 7276 Institut National de la Santéet de la Recherche Médicale U1262CBRSrue du Pr.Descottes87025 LimogesFrance INSERM u1236 UniversitéRennes 1RennesFrance

Mouse B1 B cells originate in the embryonic liver and are the major B-cell population in the peritoneal and pleural cavities.1–5 By contrast,mouse B2 B cells originate in the bone marrow and are the major B-cell population in the bone marrow,spleen,and blood.B1 and B2 B cells differ not only in their origin and locations,but also in their antigen specificity,cell surface markers,capacities for class-switch recombination(CSR)and somatic hypermutation(SHM).IgH cis-regulatory regions and,particularly,transcriptional super-enhancers are major locus regulators under both normal and pathological conditions.6,7 Important differences have been found regarding the ability of the IgH 3′regulatory region(3′RR)super-enhancer to control the B1 and B2 B-cell fate.

关键词： spleen specificity peritoneal

Impact of high-fat diet and vitamin D_3 supplementation on aortic stenosis establishment in waved-2 epidermal growth factor receptor mutant mice

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Journal of Integrative Medicine 2019年第2期17卷 107-114页

作者： Bérénice Colleville Nicolas Perzo Guillaume Avinée Ana?s Dumesnil Frederic Ziegler Paul Billoir Hélène Eltchaninoff Vincent Richard Eric Durand department of Biology Institut National de la Santé et de la Recherche Médicale U1096 (Endothélium Valvulopathies et Insuffisance Cardiaque) Normandie University Fédération Hospitalo-universitaire REMOdeling in Valvulopathy and Heart Failure department of Cardiology Rouen University Hospital department of Biology Institut National de la Santé et de la Recherche Médicale U1073 (Nutrition Inflammation et Dysfonction de l’axe Intestin-Cerveau) Normandie University institute for Clinical Biology-General Biochemistry unit Rouen University Hospital department of Vascular Hemostasis Rouen University Hospital

Objective: The use of animal models of aortic stenosis(AS) remains essential to further elucidate its pathophysiology and to evaluate new therapeutic strategies. The waved-2 mouse AS model has been proposed;data have indicated that while aortic regurgitation(AR) is effectively induced, development of AS is *** aimed to evaluate the effect of high-fat diet(HFD) and vitamin D_3 supplementation in this ***: HFD and subcutaneous vitamin D_3 injections were initiated at the age of 6 weeks until the age of 6(n = 16, 6-month treatment group) and 9(n = 11, 9-month treatment group) months. Twelve waved-2 mice without supplementation were used as control. Echocardiography was performed at 3, 6 and 9 months. Blood serum analysis(calcium, 1,25(OH)_2D_3 and cholesterol), histology and immunohistochemistry(CD-31, CD-68 and osteopontin) were evaluated at the end of the experiment(6 or 9 months).Results: Total cholesterol and 1,25(OH)_2D_3 were significantly increased relative to the control group. HFD and vitamin D_3 supplementation did result in improvements to the model, since AS was only detected in 6(15.3%) mice(2 in the 3 groups) and AR was developed in the remaining animals. Echocardiographic parameters, fibrosis, thickness, inflammation and valvular calcification, were not significantly different between the 6-month treatment and control groups. Similar results were also observed in the 9-month treatment ***: These results suggest that HFD and vitamin D_3 supplementation have no effect in the waved-2 mouse model. This model essentially mimics AR and rarely AS. Further studies are needed to find a reliable animal model of AS.

关键词： Experimental model Epidermal growth factor receptor Vitamin D3 High-fat diet Aortic stenosis Aortic regurgitation

Effect of alcohol consumption on liver stiffness measured by transient elastography

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World Journal of Gastroenterology 2013年第4期19卷 516-522页

作者： Edouard Bardou-Jacquet Ludivine Legros Draman Soro Marianne latournerie Anne Guillygomarc'h Caroline Le lan Pierre Brissot Dominique Guyader Romain Moirand Hepatology and Addictology department University Hospital PontchaillouF35000 RennesFrance institut national de la Santé et de la recherche Médicale u991 Institut Fédératif de Recherche 140University of Rennes 1F35000 RennesFrance

AIM:To determine the evolution of transient elastography(TE) in patients with alcoholic liver disease according to alcohol cessation or ***:We retrospectively selected in our local database all patients who had two TE between June 2005 and November 2010 with chronic alcohol excessive consumption and excluded those with associated cause of liver *** was performed at least one week apart by senior *** examinations with less than ten successful measures or with an interquartile range above 30% were *** retrospectively reviewed file of all patients to include only patient followed up by trained addictologist and for which definite information on alcohol consumption was *** biological parameters [aspartate amino transferase(AST),alanine amino transferase and gamma-glutamyl transpeptidase(GGT)] within 4 wk of initial and final TE were *** fibrosis score according to initial and final TE were determined with available cut-off for alcoholic liver disease and hepatitis *** and final putative fibrosis score were compared according to alcohol consumption during ***:During the study period 572 patients had TE examination for alcoholic liver disease and 79 of them had at least two ***-seven patients met our criteria with a median follow-up of 32.5 *** the end of the study,13(35%) were abstinent,and 24(65%) *** patients had liver biopsy during *** decreased significantly during follow-up in 85% of abstinent patients [median(range):-4.9(-6.1,-1.9)],leading to a modification of the putative fibrosis stage in 28%-71% of patient according to different cut-off *** relapsers TE increased in 45% and decreased in 54% of *** was no statistical difference between initial and final TE in *** the overall population,using 22.6 kPa as cut-off for cirrhosis,4 patients had cirrhosis at initial TE and 3 patients had cirrhosis at final ***

关键词： Alcohol Transient elastography Cirrhosis Fibrosis Liver biopsy Liver stiffness

Partial Beclin 1 silencing aggravates doxorubicin-and Fasinduced apoptosis in HepG2 cells

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World Journal of Gastroenterology 2006年第18期12卷 2895-2900页

作者： Fanny Daniel Agnès Legrand Dominique Pessayre Nathalie Vadrot Véronique descatoire Dominique Bernuau institut national de la Santé et de la recherche Médicale INSERMU773Centre de Recherche Bichat Beaujon CRB3BP 416F-75018ParisFrance université paris 7 denis Diderot site BichatBP 416F-75018ParisFrance

AIM： To investigate the role of Beclin 1 on the susceptibility of HepG2 cells to undergo apoptosis after anti-Fas antibody or doxorubicin treatment. MetHODS： Beclin 1 silencing was achieved using RNA interference. DNA ploidy, the percentage of apoptotic cells and the mitochondrial membrane potential were assessed by flow cytometry. Levels of Beclin 1, BCI-XL and cytochrome c, and the cleavage of poly （ADP-ribose） polymerase （PARP） were assayed by using Western blots. RESuLTS： Beclin 1 expression decreased by 75% 72 h after Beclin 1 siRNA transfection. Partial Beclin 1 silencing significantly increased the percentage of subG1 cells 24 and 40 h after treatment with doxorubicin or anti-Fas antibody, respectively, and this potentiation was abrogated by treatment with a pan-caspase inhibitor. Partial Beclin 1 silencing also increased PARP cleavage, mitochondrial membrane depolarization and cytosolic cytochrome c. The pro-apoptotic consequences of partial Beclin 1 silencing were not associated with a decline in Bcl-XL expression.CONCLuSION： Partial Beclin 1 silencing aggravates mitochondrial permeabilization and apoptosis in HepG2 cells treated with an anti-Fas antibody or with doxorubicin.

关键词： Beclin 1 Apoptosis HepG2 cells Anti-Fas antibody Doxorubicin

Artificial intelligence and omics in cancer

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Artificial Intelligence in Cancer 2020年第1期1卷 1-7页

作者： Cédric Coulouarn institut national de la sante et de la recherche medicale(Inserm) Universitéde Rennes 1Rennes F-35000France

Cancer is a major public health problem *** predictions suggest that 13 million people will die each year from cancer by ***,new ideas are urgently needed to change paradigms in the global fight against *** the last decades,artificial intelligence(AI)emerged in the field of cancer research as a new and promising *** emerging,a great potential is appreciated in AI to improve cancer diagnosis and prognosis,as well as to identify relevant therapeutics in the current era of personalized *** pipelines connecting patient-generated health data easily translatable into clinical practice to assist clinicians in decision making represents a challenging but fascinating *** algorithms are mainly fueled by multi omics data which,in the case of cancer research,have been largely derived from international cancer programs,including The Cancer Genome Atlas(TCGA).Here,I briefly review some examples of supervised and unsupervised big data derived from TCGA programs and comment on how AI algorithms have been applied to improve the management of patients with *** this context,Artificial Intelligence in Cancer journal was specifically launched to promote the development of this discipline,by serving as a forum to publish high-quality basic and clinical research articles in various fields of AI in oncology.

关键词： Omics Big data Artificial intelligence deep learning Precision medicine

Generation of obese rat model by transcription activator-like effector nucleases targeting the leptin receptor gene

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Science China(Life Sciences) 2017年第2期60卷 152-157页

作者： Yuting Chen Wenqing Lu Na Gao Yi Long Yanjiao Shao Meizhen Liu Huaqing Chen Shixin Ye Xueyun Ma Mingyao Liu Dali Li Shanghai Key laboratory of Regulatory Biology Institute of Biomedical Sciences and School of Life Sciences East China Normal University Shanghai 200241 China Ecole Normale Supérieure Institut de Biologie de l' Ecole Normale Supérieure Institut National de la Santé et de la Recherche Médicale U1024 Centre National de la Recherche Scientifique Unité Mixte de Recherche 8197 Paris F-75005 France institute of Biosciences and Technology Department of Molecular and Cellular Medicine Texas A&M University Health Science Center Houston Texas 77030 USA

The laboratory rat is a valuable mammalian model organism for basic research and drug discovery. Here we demonstrate an efficient methodology by applying transcription activator-like effector nucleases(TALENs) technology to generate Leptin receptor(Lepr) knockout rats on the Sprague Dawley(SD) genetic background. Through direct injection of in vitro transcribed m RNA of TALEN pairs into SD rat zygotes, somatic mutations were induced in two of three resulting pups. One of the founders carrying bi-allelic mutation exhibited early onset of obesity and infertility. The other founder carried a chimeric mutation which was efficiently transmitted to the progenies. Through phenotyping of the resulting three lines of rats bearing distinct mutations in the Lepr locus, we found that the strains with a frame-shifted or premature stop codon mutation led to obesity and metabolic disorders. However, no obvious defect was observed in a strain with an in-frame 57 bp deletion in the extracellular domain of Lepr. This suggests the deleted amino acids do not significantly affect Lepr structure and function. This is the first report of generating the Lepr mutant obese rat model in SD strain through a reverse genetic approach. This suggests that TALEN is an efficient and powerful gene editing technology for the generation of disease models.

关键词： TALENs Lepr knockout rat germ-line transmission

Colon cancer stemness as a reversible epigenetic state:Implications for anticancer therapies

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World Journal of Stem Cells 2019年第11期11卷 920-936页

作者： Audrey Vincent Aicha Ouelkdite-Oumouchal Mouloud Souidi Julie Leclerc Bernadette Neve Isabelle Van Seuningen Lille university Institut National de la Sante et de la Recherche MédicaleCHU LilleUMR-S 1172-Jean-Pierre Aubert Research CenterLille F-59000France department of Biochemistry and Molecular Biology Lille University HospitalLille F-59000France

The recent discovery of cancer cell plasticity,*** ability to reprogram into cancer stem cells(CSCs)either naturally or under chemotherapy and/or radiotherapy,has changed,once again,the way we consider cancer *** cancer stemness is a reversible epigenetic state rather than a genetic identity,opportunities will arise for therapeutic strategies that remodel epigenetic landscapes of ***,the systematic use of DNA methyltransferase and histone deacetylase inhibitors,alone or in combination,in advanced solid tumors including colorectal cancers,regardless of their molecular subtypes,does not seem to be the best *** this review,we first summarize the knowledge researchers have gathered on the epigenetic signatures of CSCs with the difficulty of isolating rare populations of *** raise questions about the relevant use of currently available epigenetic inhibitors(epidrugs)while the expression of numerous cancer stem cell markers are often repressed by epigenetic *** markers include the three cluster of differentiation CD133,CD44 and CD166 that have been extensively used for the isolation of colon ***,we describe current treatment strategies using epidrugs,and we hypothesize that,using correlation tools comparing associations of relevant CSC markers with chromatin modifier expression,we could identify better candidates for epienzyme targeting.

关键词： Cancer stem cells Colon cancer Epigenetics Chromatin modifying enzymes CD44 CD133 CD166

Single-cell profiling reveals the trajectories of natural killer cell differentiation in bone marrow and a stress signature induced by acute myeloid leukemia

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Cellular & Molecular Immunology 2021年第11期18卷 1290-1304页

作者： Adeline Crinier Pierre-Yves Dumas Bertrand Escalière Christelle Piperoglou laurine Gil Arnaud Villacreces Frédéric Vély Zoran Ivanovic Pierre Milpied Émilie Narni-Mancinelli Éric Vivier Aix Marseille university CNRSINSERMCentre d’Immunologie de Marseille-LuminyMarseilleFrance CHu Bordeaux Service d’Hématologie Clinique et de Thérapie CellulaireBordeauxFrance Bordeaux university BordeauxFrance institut national de la Santéet de la recherche Médicale U1035BordeauxFrance APHM Hôpital de la TimoneMarseille-ImmunopôleMarseilleFrance Établissement Français du Sang Nouvelle Aquitaine BordeauxFrance Innate Pharma Research laboratories Innate PharmaMarseilleFrance

Natural killer(NK)cells are innate cytotoxic lymphoid cells(ILCs)involved in the killing of infected and tumor *** human and mouse NK cells from the spleen and blood,we previously identified by single-cell RNA sequencing(scRNAseq)two similar major subsets,NK1 and *** the same technology,we report here the identification,by single-cell RNA sequencing(scRNAseq),of three NK cell subpopulations in human bone *** analysis identified a subset of resident CD56^(bright) NK cells,NK0 cells,as the precursor of both circulating CD56dim NK1-like NK cells and CD56^(bright) NK2-like NK cells in human bone marrow and spleen under physiological *** profiles of bone marrow NK cells from patients with acute myeloid leukemia(AML)exhibited stress-induced repression of NK cell effector functions,highlighting the profound impact of this disease on NK cell *** marrow NK cells from AML patients exhibited reduced levels of CD160,but the CD160high group had a significantly higher survival rate.

关键词： NK cells scRNASeq AML

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Neuroendocrine control of natural killer cell function through the checkpoint molecule PD-1

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Cellular & Molecular Immunology 2019年第2期16卷 109-111页

作者： Justine devulder Anne Tsicopoulos Catherine Duez Pulmonary Immunity Institut National de la SantéEt de la Recherche MédicaleU1019F-59019 LilleFrance institut Pasteur de Lille Center for Infection and Immunity of LilleF-59019 LilleFrance CNRS uMR 8204 F-59000 LilleFrance univ Lille Nord de France F-59000 LilleFrance Clinique des Maladies Respiratoires et Centre Hospitalier Régional et universitaire de Lille 59037 LilleFrance

Host defense strategies encompass resistance to reduce pathogen burden,and disease tolerance to preserve host fitness.1 Immunedriven resistance mechanisms have inevitably a negative impact on host fitness and can lead to *** tolerance limit immunopathology and therefore disease severity by preventing tissue damage or ameliorating tissue function without interfering with pathogen *** pathways cooperate to protect the *** pathways include metabolic and oxidative stress responses,2 and the interaction between neuroendocrine system and the immune system3 to favor resolution of inflammation and to prevent tissue damage.

关键词： damage killer inflammation