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| 1 | Autoimmune liver serology:Current diagnostic and clinical challenges显示文摘Liver-related autoantibodies are crucial for the correct diagnosis and classification of autoimmune liver diseas-es(AiLD),namely autoimmune hepatitis types 1 and 2(AIH-1 and 2),primary biliary cirrhosis(PBC),and the sclerosing cholangitis variants in adults and children.AIH-1 is specified by anti-nuclear antibody(ANA) and smooth muscle antibody(SMA).AIH-2 is specified by antibody to liver kidney microsomal antigen type-1(anti-LKM1) and anti-liver cytosol type 1(anti-LC1).SMA,ANA and anti-LKM antibodies can be present in de-novo AIH following liver transplantation.PBC is specified by antimitochondrial antibodies(AMA) react-ing with enzymes of the 2-oxo-acid dehydrogenase complexes(chiefly pyruvate dehydrogenase complex E2 subunit) and disease-specific ANA mainly react-ing with nuclear pore gp210 and nuclear body sp100.Sclerosing cholangitis presents as at least two variants,first the classical primary sclerosing cholangitis(PSC) mostly affecting adult men wherein the only(and non-specific) reactivity is an atypical perinuclear antineutro-phil cytoplasmic antibody(p-ANCA),also termed peri-nuclear anti-neutrophil nuclear antibodies(p-ANNA) and second the childhood disease called autoimmune sclerosing cholangitis(ASC) with serological features resembling those of type 1 AIH.Liver diagnostic serol-ogy is a fast-expanding area of investigation as new purified and recombinant autoantigens,and automatedtechnologies such as ELISAs and bead assays,become available to complement(or even compete with) tradi-tional immunofluorescence procedures.We survey for the first time global trends in quality assurance impact-ing as it does on(1) manufacturers/purveyors of kits and reagents,(2) diagnostic service laboratories that fulfill clinicians' requirements,and(3) the end-user,the physician providing patient care,who must properly interpret test results in the overall clinical context. | Dimitrios P Bogdanos Diego Vergani Pietro Invernizzi Ian R Mackay | 2008 | World Journal of Gastroenterology2008，14，21： | 40 |
| 2 | Aetiopathogenesis of autoimmune hepatitis显示文摘The histological hallmark of autoimmune hepatitis(AIH) is a dense portal mononuclear cell infiltrate that invades the surrounding parenchyma and comprises T and B lymphocytes,macrophages,and plasma cells.An unknown but powerful stimulus must be promoting the formation of this massive inflammatory cellular reaction that is likely to initiate and perpetuate liver damage.An autoimmune attack can follow different pathways to inflict damage on hepatocytes.Liver damage is likely to be orchestrated by CD4+ T lymphocytes recognizing an autoantigenic liver peptide.To trigger an autoimmune response,the peptide must be embraced by an HLA class Ⅱ molecule and presented to na?ve CD4+ T helper(Th0) cells by professional antigen presenting cells,with the co-stimulation of ligand-ligand fostering interaction between the two cells.Th0 cells become activated,differentiate into functional phenotypes according to the cytokines prevailing in the microenvironment and the nature of the antigen,and initiate a cascade of immune reactions determined by the cytokines produced by the activated T cells.Th1 cells,arising in the presence of the macrophage-derived interleukin(IL) -12,secrete mainly IL-2 and interferon-gamma(IFN-g),which activate macrophages,enhance expression of HLA classⅠ(increasing liver cell vulnerability to a CD8+ T cell cytotoxic attack),and induce expression of HLA class Ⅱ molecules on hepatocytes.Th2 cells,which differentiate from Th0 if the microenvironment is rich in IL-4,produce mainly IL-4,IL-10,and IL-13 which favour autoantibody production by B lymphocytes.Physiologically,Th1 and Th2 antagonize each other.Th17 cells,a recently described population,arise in the presence of transforming growth factor beta(TGF-β) and IL-6 and appear to have an important effector role in inflammation and autoimmunity.Theprocess of autoantigen recognition is strictly controlled by regulatory mechanisms,such as those exerted by CD4+CD25+ regulatory T cells,which derive from Th0 in the presence of TGF-β,but in the absence of IL-6.If regulatory mechanisms fail,the autoimmune attack is perpetuated.Over the past three decades different aspects of the above pathogenic scenario have been investigated.In particular,a defect in immunoregulation affecting CD4+CD25+ regulatory T cells(T-regs) has been demonstrated in AIH,particularly at diagnosis or during relapse.Advances in the study of autoreactive T cells have occurred mostly in AIH type 2,since the knowledge that CYP2D6 is the main autoantigen has enabled the characterization of both CD4 and CD8 T cells targeting this cytochrome.CD4 T cells from patients with type 2 AIH positive for the predisposing HLA allele DRB10701 recognize seven regions of CYP2D6,five of which are also recognized by CD8 T cells.High numbers of IFN-g producing CD4 T cells and CD8 T cells are associated with biochemical evidence of liver damage,suggesting a combined cellular immune attack. | Diego Vergani Giorgina Mieli-Vergani | 2008 | World Journal of Gastroenterology2008，14，21： | 21 |
| 3 | Autoimmune hepatitis: standard treatment and systematic review of alternative treatments显示文摘Autoimmune hepatitis is a rare chronic inflammatory liver disease,affecting all ages,characterised by elevated transaminase and immunoglobulin G levels,positive autoantibodies,interface hepatitis at liver histology and good response to immunosuppressive treatment. If untreated,it has a poor prognosis. The aim of this review is to summarize the evidence for standard treatment and to provide a systematic review on alternative treatments for adults and children. Standard treatment is based on steroids and azathioprine,and leads to disease remission in 80%-90% of patients. Alternative first line treatment has been attempted with budesonide or cyclosporine,but their superiority compared to standard treatment remains to be demonstrated. Second-line treatments are needed for patients not responding or intolerant to standard treatment. No randomized controlled trials have been performed for second-line options. Mycophenolate mofetil is the most widely used second-line drug,and has good efficacy particularly for patients intolerant to azathioprine,but has the major disadvantage of being teratogenic. Only few and heterogeneous data on cyclosporine,tacrolimus,everolimus and sirolimus are available. More recently,experience with the anti-tumour necrosis factoralpha infliximab and the anti-CD20 rituximab has been published,with ambivalent results; these agents may have severe side-effects and their use should be restricted to specialized centres. Clinical trials with new therapeutic options are ongoing. | Benedetta Terziroli Beretta-Piccoli Giorgina Mieli-Vergani Diego Vergani | 2017 | World Journal of Gastroenterology2017，23，33： | 20 |
| 4 | Silybin counteracts lipid excess and oxidative stress in cultured steatotic hepatic cells显示文摘AIM: To investigate in vitro the therapeutic effect and mechanisms of silybin in a cellular model of hepatic steatosis.METHODS: Rat hepatoma Fa O cells were loaded with lipids by exposure to 0.75 mmol/L oleate/palmitate for 3 h to mimic liver steatosis. Then, the steatotic cells were incubated for 24 h with different concentrations(25 to 100 μmol/L) of silybin as phytosome complex with vitamin E. The effects of silybin on lipid accumulation and metabolism, and on indices of oxidative stress were evaluated by absorption and fluorescence microscopy, quantitative real-time PCR, Western blot, spectrophotometric and fluorimetric assays.RESULTS: Lipid-loading resulted in intracellular triglyceride(TG) accumulation inside lipid droplets, whose number and size increased. TG accumulation was mediated by increased levels of peroxisome proliferator-activated receptors(PPARs) and sterol regulatory element-binding protein-1c(SREBP-1c). The lipid imbalance was associated with higher production of reactive oxygen species(ROS) resulting in increased lipid peroxidation, stimulation of catalase activity and activation of nuclear factor kappa-B(NF-κB). Incubation of steatotic cells with silybin 50 μmol/L significantly reduced TG accumulation likely by promoting lipid catabolism and by inhibiting lipogenic pathways, as suggested by the changes in carnitine palmitoyltransferase 1(CPT-1), PPAR and SREBP-1c levels. The reduction in fat accumulation exerted by silybin in the steatotic cells was associated with the improvement of the oxidative imbalance caused by lipid excess as demonstrated by the reduction in ROS content, lipid peroxidation, catalase activity and NF-κB activation.CONCLUSION: We demonstrated the direct antisteatotic and anti-oxidant effects of silybin in steatotic cells, thus elucidating at a cellular level the encouraging results demonstrated in clinical and animal studies. | Giulia Vecchione Elena Grasselli Adriana Voci Francesca Baldini Ignazio Grattagliano David QH Wang Piero Portincasa Laura Vergani | 2016 | World Journal of Gastroenterology2016，22，26： | 13 |
| 5 | Role of monocytes and macrophages in experimental and human acute liver failure显示文摘Acute liver failure (ALF) is a devastating clinical syndrome characterised by progressive encephalopathy, coagulopathy, and circulatory dysfunction, which commonly leads to multiorgan failure and death. Central to the pathogenesis of ALF is activation of the immune system with mobilisation of cellular effectors and massive production of cytokines. As key components of the innate immune system, monocytes and macrophages are postulated to play a central role in the initiation, progression and resolution of ALF. ALF in humans follows a rapidly progressive clinical course that poses inherent difficulties in delineating the role of these pivotal immune cells. Therefore, a number of experimental models have been used to study the pathogenesis of ALF. Here we consider the evidence from experimental and human studies of ALF on the role of monocytes and macrophages in acute hepatic injury and the ensuing extrahepatic manifestations, including functional monocyte deactivation and multiple organ failure. | Lucia A Possamai Charalambos Gustav Antoniades Quentin M Anstee Alberto Quaglia Diego Vergani Mark Thursz Julia Wendon | 2010 | World Journal of Gastroenterology2010，16，15： | 12 |
| 6 | Autoimmmune hepatitis显示文摘Autoimmune hepatitis(AIH)is a T-cell mediated,inflammatory liver disease affecting all ages and characterized by female preponderance,elevated serum transaminase and immunoglobulin G levels,positive circulating autoantibodies,and presence of interface hepatitis at liver histology.AIH type 1,affecting both adults and children,is defined by positive anti-nuclear and/or antismooth muscle antibodies,while type 2 AIH,affecting mostly children,is defined by positive anti-liver-kidney microsomal type 1 and/or anti-liver cytosol type 1 antibody.While the autoantigens of type 2 AIH are well defined,being the cytochrome P4502D6(CYP2D6)and the formiminotransferase cyclodeaminase(FTCD),in type 1 AIH they remain to be identified.AIH-1 predisposition is conferred by possession of the MHC class II HLA DRB1*03 at all ages,while DRB1*04 predisposes to late onset disease;AIH-2 is associated with possession of DRB1*07 and DRB1*03.The majority of patients responds well to standard immunosuppressive treatment,based on steroid and azathioprine;second-and third-line drugs should be considered in case of intolerance or insufficient response.This review offers a comprehensive overview of pathophysiological and clinical aspects of AIH. | Benedetta Terziroli Beretta-Piccoli Giorgina Mieli-Vergani Diego Vergani | 2022 | Cellular & Molecular Immunology2022，19，2： | 7 |
| 7 | Incubation Phase of Acute Hepatitis B in Man: Dynamic of Cellular Immune Mechanisms显示文摘 | George J.M. Webster Stephanie Reignat Mala K. Maini Simon A. Whalley Graham S. Ogg Abigail King David Brown Peter L. Amlot Roger Williams Diego Vergani Geoffrey M. Dusheiko Antonio Bertoletti | 2000 | Hepatology2000，，5： | 4 |
| 8 | Autoimmune paediatric liver disease显示文摘Liver disorders with a likely autoimmune pathogenesis in childhood include autoimmune hepatitis(AIH),autoimmune sclerosing cholangitis(ASC),and de novo AIH after liver transplantation.AIH is divided into two subtypes according to seropositivity for smooth muscle and/or antinuclear antibody(SMA/ANA,type 1) or liver kidney microsomal antibody(LKM1,type 2).There is a female predominance in both.LKM1 positive patients tend to present more acutely,at a younger age,and commonly have partial IgA deficiency,while duration of symptoms before diagnosis,clinical signs,family history of autoimmunity,presence of associated autoimmune disorders,response to treatment,and long-term prognosis are similar in both groups.The most common type of paediatric sclerosing cholangitis is ASC.The clinical,biochemical,immunological,and histological presentation of ASC is often indistinguishable from that of AIH type 1.In both,there are high IgG,non-organ specific autoantibodies,and interface hepatitis.Diagnosis is made by cholangiography.Children with ASC respond to immunosuppression satisfactorily and similarly to AIH in respect to remission and relapse rates,times to normalization of biochemical parameters,and decreased inflammatory activity on follow up liver biopsies.However,the cholangiopathy can progress.There may be evolution from AIH to ASC over the years,despite treatment.De novo AIH after liver transplantation affects patients not transplanted for autoimmune disorders and is strikingly reminiscent of classical AIH,including elevated titres of serum antibodies,hypergammaglobulinaemia,and histological findings of interface hepatitis,bridging fibrosis,and collapse.Like classical AIH,it responds to treatment with prednisolone and azathioprine.De novo AIH postliver transplantation may derive from interference by calcineurin inhibitors with the intrathymic physiological mechanisms of T-cell maturation and selection.Whether this condition is a distinct entity or a form of atypical rejection in individuals susceptible to the development of autoimmune phenomena is unclear.Whatever its etiology,the recognition of this potentially life-threatening syndrome is important since its management differs from that of standard anti-rejection therapy. | Giorgina Mieli-Vergani Diego Vergani | 2008 | World Journal of Gastroenterology2008，14，21： | 3 |
| 9 | Diagnosis and management of autoimmune hepatitis显示文摘 | Michael P. Manns Albert J. Czaja James D. Gorham Edward L. Krawitt Giorgina Mieli‐Vergani Diego Vergani John M. Vierling | 2010 | Hepatology2010，，： | 3 |
| 10 | Lipid lowering effects of iodothyronines:In vivo and in vitro studies on rat liver显示文摘Non-alcoholic fatty liver disease(NAFLD) is emerging as one of the most common liver diseases,leading to the increasing interest for new therapeutic approaches for its treatment.NAFLD primarily depends on a hypercaloric and/or unbalanced diet leading to overweight and obesity.The liver,in fact,plays a central role in lipid metabolism by importing free fatty acids from the blood and synthesizing,storing,oxidizing and exporting lipids.Furthermore,the liver is the target for the thyroid hormones,thyroxine(T4) and 3,3',5-triiodo-L-thyronine(T3),that stimulate the basal metabolic rate and lead to body weight loss.In the last decade,other iodothyronines have been shown to possess biological relevance and play some thyromimetic activities; in particular,3,5-diiodo-L-thyronine(T2) gained large interest.The global effect of iodothyronines on liver lipid metabolism results from the balance between direct and indirect actions on the hepatocyte,leading to stimulation of lipid synthesis,oxidation and autophagy.In this review,the results so far obtained on both in vivo and in vitro models of hepatosteatosis are summarized in order to obtain an updated picture of the lipid-lowering effects of iodothyronines on mammalian liver. | Laura Vergani | 2014 | World Journal of Hepatology2014，6，4： | 3 |
| 11 | Direct effects of iodothyronines on excess fat storage in rat hepatocytes显示文摘 | Elena Grasselli Adriana Voci Laura Canesi Rita De Matteis Fernando Goglia Federica Cioffi Emilia Fugassa Gabriella Gallo Laura Vergani | 2010 | Journal of Hepatology2010，，6： | 2 |
| 12 | IgG3抗体与线粒体主要自身抗原决定簇及乳酸杆菌抗原位点的交叉反应是原发胆汁性肝硬化的特征 | Bogdanos D.-P. Baum H. Okamoto M. D. Vergani 徐瑞 | 2005 | 世界核心医学期刊文摘(胃肠病学分册)2005，0，11： | 2 |
| 13 | Autoimmune Hepatitis After Liver Transplantation显示文摘 | Rodrigo Liberal Maria Serena Longhi Charlotte R. Grant Giorgina Mieli–Vergani Diego Vergani | 2012 | Clinical Gastroenterology and Hepatology2012，，4： | 2 |
| 14 | Fetal arrhythmias : natural history andmanagement显示文摘 | Vergani P Mariani E Ciriello E | 2005 | Ultrasound Med Biol2005，31，1： | 1 |
| 15 | Predictors of adverse perinatal outcome in twins delivered at <?37 weeks显示文摘 | Patrizia Vergani Anna Locatelli Marta Ratti Antonietta Scian Giulia Zangheri John Pezzullo Alessandro Ghidini | 2004 | Journal of Maternal-Fetal and Neonatal Medicine2004，，6： | 1 |
| 16 | Human skeletal muscle atrophy in amyotrophic lateral sclerosis reveals a reduction in Akt and an increase in atrogin-1显示文摘 | Léger B Vergani L Sorarù G | 2006 | FASEB J2006，20，3： | 1 |
| 17 | State of the art in thora- cospic surgery: a personal experience of 2000 videothoracoscopic procedures and an overview of the literature 显示文摘 | Roviaro GC Varoli F Vergani C | 2002 | Surg Endosc2002，16，6： | 1 |
| 18 | Hepatic iron overload in patients with chronieal viral hepatitis: role of HFE gene mutation 显示文摘 | Pipemo A Vergani A | 1998 | Hepatology1998，28，4： | 1 |
| 19 | Effect of disinfectants on the hardness and roughness of reline acrylic resins显示文摘 | Azevedo A Machado AL Vergani CE | 2006 | J Prosthodont2006，15，4： | 1 |
| 20 | Efects of growth hormone and cadmium on the transcription regulation of two metallothionein isoforms 显示文摘 | Vergani L Lanza C Borghi C | 2007 | Mol Cell Endocrinol2007，263，12： | 1 |
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