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Tumor necrosis family receptor superfamily member 9/tumor necrosis factor receptor-associated f

World Journal of Hepatology 2020年第10期12卷 754-765页

作者： Julia Peña-Asensio eduardo sanz-de-villalobos Joaquín Miquel Juan Ramón Larrubia department of Systems Biology Guadalajara University Hospital.University of AlcaláGuadalajara E-19002GuadalajaraSpain Translational Hepatology Unit Guadalajara University HospitalUniversity of AlcaláGuadalajara E-19002GuadalajaraSpain

Hepatitis C virus(HCV)infection is an excellent immunological model for understanding the mechanisms developed by non-cytopathic viruses and tumors to evade the adaptative immune response.The antigen-specific cytotoxic T cell response is essential for keeping HCV under control,but during persistent infection,these cells become exhausted or even deleted.The exhaustion process is progressive and depends on the infection duration and level of antigenemia.During high antigenic load and long duration of infection,T cells become extremely exhausted and ultimately disappear due to apoptosis.The development of exhaustion involves the impairment of positive co-stimulation induced by regulatory cytokines,such as transforming growth factor beta 1.This cytokine downregulates tumor necrosis factor receptor(TNFR)-associated factor 1(TRAF1),the signal transducer of the T cell co-stimulatory molecule TNFR superfamily member 9(known as 4-1BB).This impairment correlates with the low reactivity of T cells and an exhaustion phenotype.Treatment with interleukin-7 in vitro restores TRAF1 expression and rescues T cell effector function.The process of TRAF1 loss and its in vitro recovery is hierarchical,and more affected by severe disease progression.In conclusion,TRAF1 dynamics on T cells define a new pathogenic model that describes some aspects of the natural history of HCV,and sheds light on novel immunotherapy strategies for chronic viral infections and cancer.

关键词： Hepatitis C virus Tumor necrosis factor receptor-associated factor 1 CD8 Exhaustion Tumor necrosis family receptor superfamily member 9 Chronic hepatitis

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Costimulatory molecule programmed death-1 in the cytotoxic response during chronic hepatitis C

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World Journal of Gastroenterology 2009年第41期15卷 5129-5140页

作者： Juan Ramón Larrubia Selma Benito-Martínez Joaquín Miquel Miryam Calvino eduardo sanz-de-villalobos Trinidad Parra-Cid Translational Hepatology Unit Guadalajara University Hospital University of Alcalá

Hepatitis C virus (HCV)-specific CD8+ T cells play an important role in the resolution of HCV infection. Nevertheless, during chronic hepatitis C these cells lack their effector functions and fail to control the virus. HCV has developed several mechanisms to escape immune control. One of these strategies is the upregulation of negative co-stimulatory molecules such us programmed death-1 (PD-1). This molecule is upregulated on intrahepatic and peripheral HCV-specific cytotoxic T cells during acute and chronic phases of the disease, whereas PD-1 expression is low in resolved infection. PD-1 expressing HCV-specific CD8+ T cells are exhausted with impairment of several effector mechanisms, such as: type-1 cytokine production, expansion ability after antigen encounter and cytotoxic ability. However, PD-1 associated exhaustion can be restored by blocking the interaction between PD-1 and its ligand (PD-L1). After this blockade, HCV-specificCD8+ T cells reacquire their functionality. Nevertheless, functional restoration depends on PD-1 expression level. High PD-1-expressing intrahepatic HCV-specific CD8+ T cells do not restore their effector abilities after PD-1/PD-L1 blockade. The mechanisms by which HCV is able to induce PD-1 up-regulation to escape immune control are unknown. Persistent TCR stimulation by a high level of HCV antigens could favour early PD-1 induction, but the interaction between HCV core protein and gC1q receptor could also participate in this process. The PD-1/PD-L1 pathway modulation could be a therapeutic strategy, in conjunction with the regulation of others co-stimulatory pathways, in order to restore immune response against HCV to succeed in clearing the infection.

关键词：共刺激分子程序化死亡丙型肝炎毒性反应慢性细胞

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Role of T cell death in maintaining immune tolerance during persistent viral hepatitis

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World Journal of Gastroenterology 2013年第12期19卷 1877-1889页

作者： Juan Ramón Larrubia Megha Uttam Lokhande Silvia García-Garzón Joaquín Miquel Dolores Subirá eduardo sanz-de-villalobos Translational Hepatology Unit Guadalajara University Hospital University of Alcalá

Virus-specific T cells play an important role in the resolution of hepatic infection. However, during chronic hepatitis infection these cells lack their effector functions and fail to control the virus. Hepatitis B virus and hepatitis C virus have developed several mechanisms to generate immune tolerance. One of these strategies is the depletion of virus-specific T cells by apoptosis. The immunotolerogenic liver has unique property to retain and activate na ve T cell to avoid the over reactivation of immune response against antigens which is exploited by hepatotropic viruses to persist. The deletion of the virus-specific T cells occurs by intrinsic (passive) apoptotic mechanism. The pro-apoptotic molecule Bcl-2 interacting mediator (Bim) has attracted increasing attention as a pivotal involvement in apoptosis, as a regulator of tissue homeostasis and an enhancer for the viral persistence. Here, we reviewed our current knowledge on the evidence showing critical role of Bim in viral-specific T cell death by apoptotic pathways and helps in the immune tolerance.

关键词： T cell death Specific cytotoxic T lymphocytes Hepatitis C virus immune tolerance Apoptosis Bcl-2 interacting mediator Liver tolerance Apoptotic pathways Viral hepatitis

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Is it possible to stop nucleos(t)ide analogue treatment in chronic hepatitis B patients?

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World Journal of Gastroenterology 2018年第17期24卷 1825-1838页

作者： Elia Moreno-Cubero Robert T Sánchez del Arco Julia Pena-Asensio eduardo sanz de villalobos Joaquín Míquel Juan Ramón Larrubia Translational Hepatology Unit Guadalajara University HospitalUniversity of AlcaláGuadalajara 19002Spain Internal Medicine Service Guadalajara University HospitalUniversity of AlcaláGuadalajara 19002Spain department of Biology of Systems University of AlcaláAlcaláde Henares(Madrid)28805Spain department of Medicine and Medical Specialties University of AlcaláAlcaláde Henares(Madrid)28805Spain

Chronic hepatitis B(CHB) remains a challenging global health problem, with nearly one million related deaths per year. Nucleos(t)ide analogue(NA) treatment suppresses viral replication but does not provide complete cure of the hepatitis B virus(HBV) infection. The accepted endpoint for therapy is the loss of hepatitis B surface antigen(HBs Ag), but this is hardly ever achieved. Therefore, indefinite treatment is usually required. Many different studies have evaluated NA therapy discontinuation after several years of NA treatment and before HBs Ag loss. The results have indicated that the majority of patients can remain off therapy, with some even reaching HBs Ag seroconversion. Fortunately, this strategy has proved to be safe, but it is essential to consider the risk of liver damage and other comorbidities and to ensure aclose follow-up of the candidates before considering this strategy. Unanswered questions remain, namely in which patients could this strategy be effective and what is the optimal time point at which to perform it. To solve this enigma, we should keep in mind that the outcome will ultimately depend on the equilibrium between HBV and the host's immune system. Viral parameters that have been described as good predictors of response in HBe Ag(+) cases, have proven useless in HBe Ag(-) ones. Since antiviral immunity plays an essential role in the control of HBV infection, we sought to review and explain potential immunological biomarkers to predict safe NA discontinuation in both groups.

关键词： CD8 Lamivudine Nucleos(t)ide analogues Tenofovir Chronic hepatitis B Entecavir hepatitis B virus Treatment cessation

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Hepatitis C virus-specific cytotoxic T cell response restoration after treatment-induced hepatitis C virus control

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World Journal of Gastroenterology 2015年第12期21卷 3480-3491页

作者： Juan-Ramón Larrubia Elia Moreno-Cubero Joaquín Miquel eduardo sanz-de-villalobos Translational Hepatology Unit Guadalajara University Hospital University of Alcalá department of Medicine and Medical Specialties University of Alcalá department of Biology of Systems University of Alcalá

Hepatitis C virus(HCV)-specific cytotoxic T cell(CTL) response plays a major role in viral control during spontaneous infection resolution. These cells develop an exhausted and pro-apoptotic status during chronic onset, being unable to get rid of HCV. The role of this response in contributing to sustained viral response(SVR) after anti-HCV is controversial. Recent studies show that after successful interferon-based anti-HCV treatment, HCV traces are still detectable and this correlates with a peak of HCV-specific CTL response activation, probably responsible for maintaining SVR by subsequent complete HCV clearing. Moreover, SVR patients' serum is still able to induce HCV infection in na?ve chimpanzees, suggesting that the infection could be under the control of the immune system after a successful treatment, being transmissible in absence of this adaptive response. At least theoretically, treatmentinduced viral load decrease could allow an effective HCV-specific CTL response reestablishment. This effect has been recently described with anti-HCV interferonfree regimes, based on direct-acting antivirals. Nevertheless, this is to some extent controversial with interferon-based therapies, due to the detrimental immunoregulatory α-interferon effect on T cells. Moreover, HCV-specific CTL response features during anti-HCV treatment could be a predictive factor of SVR that could have clinical implications in patient management. In this review, the recent knowledge about the role of HCV-specific CTL response in the development of SVR after anti-HCV treatment is discussed.

关键词： Hepatitis C virus Chronic hepatitis Hepatitis C vi

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Role of chemokines and their receptors in viral persistence and liver damage during chronic hepatitis C virus infection

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World Journal of Gastroenterology 2008年第47期14卷 7149-7159页

作者： Juan R Larrubia Selma Benito-Martínez Miryam Calvino eduardo sanz-de-villalobos Trinidad Parra-Cid department of Gastroenterology Guadalajara University HospitalUniversity of AlcaláDonante de Sangre st.19002 GuadalajaraSpain Guadalajara University Hospital University of AlcaláDonante de Sangre st.19002 GuadalajaraSpain

Chemokines produced in the liver during hepatitis C virus(HCV) infection induce migration of activated T cells from the periphery to infected parenchyma.The milieu of chemokines secreted by infected hepatocytes is predominantly associated with the T-helper cell/Tc1 T cell(Th1/Tc1) response.These chemokines consist of CCL3(macrophage inflammatory protein-1α;MIP-1α),CCL4(MIP-1β),CCL5(regulated on activation normal T cell expressed and secreted;RANTES),CXCL10(interferon-γ-inducible protein-10;IP-10),CXCL11(interferon-inducible T-cell α chemoattractant;I-TAC),and CXCL9(monokine induced by interferon γ;Mig) and they recruit T cells expressing either CCR5 or CXCR3 chemokine receptors.Intrahepatic and peripheral blood levels of these chemokines are increased during chronic hepatitis C.The interaction between chemokines and their receptors is essential in recruiting HCV-specific T cells to control the infection.When the adaptive immune response fails in this task,non-specific T cells without the capacity to control the infection are also recruited to the liver,and these are ultimately responsible for the persistent hepatic damage.The modulation of chemokine receptor expression and chemokine secretion could be a viral escape mechanism to avoid specific T cell migration to the liver during the early phase of infection,and to maintain liver viability during the chronic phase,by impairing non-specific T cell migration.Some chemokines and their receptors correlate with liver damage,and CXCL10(IP-10) and CXCR3 levels have shown a clinical utility as predictors of treatment response outcome.The regulation of chemokines and their receptors could be a future potential therapeutic target to decrease liver inflammation and to increase specific T cell migration to the infected liver.

关键词：丙肝病毒性肝炎发病原理肝脏损伤

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Adaptive immune response during hepatitis C virus infection

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World Journal of Gastroenterology 2014年第13期20卷 3418-3430页

作者： Juan Ramon Larrubia Elia Moreno-Cubero Megha Uttam Lokhande Silvia Garcia-Garzon Alicia Lazaro Joaquin Miquel Cristian Perna eduardo sanz-de-villalobos Translational Hepatology Unit Guadalajara University HospitalUniversity of AlcalaE-19002 GuadalajaraSpain department of Medicine and Medical Specialities School of MedicineUniversity of AlcalaE-28801 Alcala de HenaresSpain

Hepatitis C virus(HCV)infection affects about 170 million people worldwide and it is a major cause of liver cirrhosis and hepatocellular carcinoma.HCV is a hepatotropic non-cytopathic virus able to persist in a great percentage of infected hosts due to its ability to escape from the immune control.Liver damage and disease progression during HCV infection are driven by both viral and host factors.Specifically,adaptive immune response carries out an essential task in controllingnon-cytopathic viruses because of its ability to recognize infected cells and to destroy them by cytopathic mechanisms and to eliminate the virus by non-cytolytic machinery.HCV is able to impair this response by several means such as developing escape mutations in neutralizing antibodies and in T cell receptor viral epitope recognition sites and inducing HCV-specific cytotoxic T cell anergy and deletion.To impair HCV-specific T cell reactivity,HCV affects effector T cell regulation by modulating T helper and Treg response and by impairing the balance between positive and negative co-stimulatory molecules and between pro-and antiapoptotic proteins.In this review,the role of adaptive immune response in controlling HCV infection and the HCV mechanisms to evade this response are reviewed.

关键词： Hepatitis C, Adaptive immune response, Hepatitis C virus-specific cytotoxic T cells, Hepatitis C virus-specific T helper cells, T regs, Hepatitis C virus escape mutations, Anergy, Apoptosis, Chemotaxis

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The first record of dermochelyid turtles in the Eocene of Tierra del Fuego:new insights on the evolution of the Weddellian faunas

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Advances in Polar Science 2024年第1期35卷 63-77页

作者： Paula BONA Juliana STERLI Marcelo Saúl de la FUENTE eduardo OLIVERO Marta S.FERNÁNdeZ Marcelo REGUERO División Paleontología Vertebrados Museo de La Plata-Anexo IIFacultad de Ciencias Naturales y MuseoUniversidad Nacional de La PlataLa Plata B1900FWAArgentina Consejo Nacional de Investigaciones Científicas y Técnicas(CONICET) Ciudad Autónoma de Buenos Aires C1425FQBArgentina Museo Paleontológico Egidio Feruglio Trelew U9100Argentina Instituto de Evolución Ecología Histórica y Ambiente-CONICETSan Rafael CP5600Argentina Centro Austral de Investigaciones Científicas-CONICET Universidad Nacional de Tierra del FuegoUshuaia CP 9410Argentina División Paleontología Vertebrados Museo de La PlataUniversidad Nacional de La PlataLa Plata B1900FWAArgentina

The Antarctic Paleogene marine fossil record has been the key to reconstructing the evolution of the Weddellian Sea and final dismemberment of Southern Gondwana.In this context,Eocene marine vertebrates from Seymour(Marambio)Island have provided valuable information.We present the first Eocene record of marine reptiles from the southern Atlantic Coast of South America.This corresponds to several postcranial turtle remains represented by a proximal end of the right humerus,three caudal and one thoracic vertebrae,a fragment of the left pubis,and ten ossicles of the dorsal carapace,coming from the Leticia Formation(late-mid Eocene)at Cabo Tiburones,Tierra del Fuego,Argentina.These materials show severalfeatures such as the size and general morphology of the humerus and vertebrae,and the presence of relatively small,irregular,smooth,and unkeeled ossicles,which allow us to assign them to dermochelyidae indet.dermochelyids are a cosmopolitan group ofcryptodiran turtles,registered from the late Cretaceous up to the recent,with some physiological-biological peculiarities(e.g.,endothermy and an exclusive jellyfish-based diet)and characterized by the presence of an osseous carapace formed by ossicles.The new finding from the Leticia Formation is an addition to the scarce and extremely fragmentary record of Eocene dermochelyids from the southern seas like those from the La Meseta and Submeseta formations(Antarctica)and the Waihao and Burnside formations(New Zealand).This new information allows us to discuss the presence of these turtles in such high latitudes in the past and its implication in the evolution of the Weddellian fauna.

关键词： marine reptiles sea turtles dermochelyidae Paleogene La Meseta Formation Submeseta Formation Leticia Formation

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Rifaximin on epigenetics and autophagy in animal model of hepatocellular carcinoma secondary to metabolic-dysfunction associated steatotic liver disease

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World Journal of Hepatology 2024年第1期16卷 75-90页

作者： Matheus Truccolo Michalczuk Larisse Longo Melina Belén Keingeski Bruno de Souza Basso Gabriel Tayguara Silveira Guerreiro Jessica T Ferrari Joséeduardo Vargas Cláudia P Oliveira Carolina Uribe-Cruz Carlos Thadeu Schmidt Cerski eduardo Filippi-Chiela Mário ReisÁlvares-da-Silva Division of Gastroenterology Hospital de Clínicas de Porto AlegrePorto Alegre 90035-903Rio Grande do SulBrazil Graduate Program in Gastroenterology and Hepatology Universidade Federal do Rio Grande do SulPorto Alegre 90035-003Rio Grande do SulBrazil Experimental Laboratory of Hepatology and Gastroenterology Hospital de Clínicas de Porto AlegrePorto Alegre 90035-903Rio Grande do SulBrazil Laboratory of Inflammatory and Neoplastic Cells Universidade Federal do ParanáParaná81530900Brazil department of Gastroenterology(LIM07) Faculdade de Medicina da Universidade de São PauloSão Paulo 01246903Brazil Facultad de Ciencias de la Salud Universidad Católica de las MisionesPosadasMisiones 3300Argentina Unit of Surgical Pathology Hospital de Clinicas de Porto AlegrePorto Alegre 90035-903Rio Grande do SulBrazil Center of Biotechnology Universidade Federal do Rio Grande do SulPorto Alegre 90035-003Rio Grande do SulBrazil department of Morphological Sciences Universidade Federal do Rio Grande do SulPorto Alegre 90.050-170Rio Grande do SulBrazil Conselho Nacional de desenvolvimento Científico e Tecnológico(CNPq) Conselho Nacional de Desenvolvimento Científico e Tecnológico(CNPq)ResearcherBrasília 71.605-001Brazil

BACKGROUND Prevalence of hepatocellular carcinoma(HCC)is increasing,especially in patients with metabolic dysfunctionassociated steatotic liver disease(MASLD).AIM To investigate rifaximin(RIF)effects on epigenetic/autophagy markers in animals.METHODS Adult Sprague-Dawley rats were randomly assigned(n=8,each)and treated from 5-16 wk:Control[standard diet,water plus gavage with vehicle(Veh)],HCC[high-fat choline deficient diet(HFCD),diethylnitrosamine(deN)in drinking water and Veh gavage],and RIF[HFCD,deN and RIF(50 mg/kg/d)gavage].Gene expression of epigenetic/autophagy markers and circulating miRNAs were obtained.RESULTS All HCC and RIF animals developed metabolic-dysfunction associated steatohepatitis fibrosis,and cirrhosis,but three RIF-group did not develop HCC.Comparing animals who developed HCC with those who did not,miR-122,miR-34a,tubulin alpha-1c(Tuba-1c),metalloproteinases-2(Mmp2),and metalloproteinases-9(Mmp9)were significantly higher in the HCC-group.The opposite occurred with Becn1,coactivator associated arginine methyltransferase-1(Carm1),enhancer of zeste homolog-2(Ezh2),autophagy-related factor LC3A/B(Map1 Lc3b),and p62/sequestosome-1(p62/SQSTM1)-protein.Comparing with controls,Map1 Lc3b,Becn1 and Ezh2 were lower in HCC and RIF-groups(P0.05).miR-122 was higher in HCC,and miR-34a in RIF compared to controls(P0.05).CONCLUSION RIF might have a possible beneficial effect on preventing/delaying liver carcinogenesis through epigenetic modulation in a rat model of MASLD

关键词： Animal model Autophagy Epigenetic Hepatocellular carcinoma Metabolic dysfunction-associated steatotic liver disease Rifaximin

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How inflammation influences psychiatric disease

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World Journal of Psychiatry 2024年第3期14卷 342-349页

作者： eduardo Ferat-Osorio JoséLuis Maldonado-García Lenin Pavón División de Investigación Clínica de la Coordinación de Investigación en Salud Instituto Mexicano del Seguro SocialMexico City 06720Mexico departamento de Bioquímica Facultad de MedicinaUniversidad Nacional Autónoma de MéxicoCoyoacán 04510Ciudad de MéxicoMexico departamento de Inmunología Escuela Nacional de Ciencias BiológicasInstituto Politécnico NacionalMexico City 11340Mexico Laboratorio de Psicoinmunología Instituto Nacional de Psiquiatría Ramón de la Fuente MuñizMexico City 14370Mexico

Recent studies highlight the strong correlation between infectious diseases and the development of neuropsychiatric disorders.In this editorial,we comment on the article“Anti-infective therapy durations predict psychological stress and laparoscopic surgery quality in pelvic abscess patients”by Zhang et al,published in the recent issue of the World Journal of Psychiatry 2023;13(11):903-911.Our discussion highlighted the potential consequences of anxiety,depression,and psychosis,which are all linked to bacterial,fungal,and viral infections,which are relevant to the impact of inflammation on the sequelae in mental health as those we are observing after the coronavirus disease 2019 pandemic.We focus specifically on the immune mechanisms triggered by inflammation,the primary contributor to psychiatric complications.Importantly,pathophysiological mechanisms such as organ damage,post-injury inflammation,and infectioninduced endocrine alterations,including hypocortisolism or autoantibody formation,significantly contribute to the development of chronic low-grade inflammation,promoting the emergence or development of psychiatric alterations in susceptible individuals.As inflammation can have long-term effects on patients,a multidisciplinary treatment plan can avoid complications and debilitating health issues,and it is crucial to recognize and address the mental health implications.

关键词： Inflammation infection depression Pelvic inflammatory disease Psychiatric complication

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