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1. Incidence and predictors of hepatocellular carcinoma in patients with autoimmune hepatitis

Author

van Gerven, N., van Erpecum, K., Ouden, J den, Brouwer, J., Vrolijk, J., Gevers, T.J., Drenth, J., Guichelaar, M., Bouma, G., Schreuder, T.C.M.A., van der Wouden, E.J., Baak, L.C., Stadhouders, P., Klemt-Kropp, M., Verhagen, M., Bhalla, A., Kuijvenhoven, J., Almasio, P., Alvarez, F., Andrade, R., Arikan, C., Assis, D., Bardou-Jacquet, E., Biewenga, M., Cancado, E., Cazzagon, N., Chazouillères, O., Colloredo, G., Cuarterolo, M., Dalekos, G., Debray, D., Robles-Díaz, M., Dyson, J., Efe, C., Engel, B., Ferri, S., Fontana, R., Gatselis, N., Gerussi, A., Halilbasic, E., Halliday, N., Heneghan, M., Hirschfield, G., van Hoek, B., Hørby Jørgensen, M., Indolfini, G., Iorio, R., Invernizzi, P., Jeong, S., Jones, D., Kelly, D., Kerkar, N., Lacaille, F., Lammert, C., Leggett, B., Lenzi, M., Levy, C., Liberal, R., Lleo, A., Lohse, A., Lopez, S. Ines, de Martin, E., McLin, V., Mieli-Vergani, G., Milkiewicz, P., Mohan, N., Muratori, L., Nebbia, G., van Nieuwkerk, C., Oo, Y., Ortega, A., Páres, A., Pop, T., Pratt, D., Purnak, T., Ranucci, G., Rushbrook, S., Schramm, C., Stättermayer, A., Swain, M., Tanaka, A., Taubert, R., Terrabuio, D., Terziroli, B., Trauner, M., Valentino, P., van den Brand, F., Vergani, D., Villamil, A., Wahlin, S., Ytting, H., Zachou, K., Zeniya, M., Colapietro, Francesca, Maisonneuve, Patrick, Lytvyak, Ellina, Beuers, Ulrich, Verdonk, Robert C., van der Meer, Adriaan J., van Hoek, Bart, Kuiken, Sjoerd D., Brouwer, Johannes T., Muratori, Paolo, Aghemo, Alessio, Carella, Francesco, van den Berg, Ad P., Zachou, Kalliopi, Dalekos, George N., Di Zeo-Sánchez, Daniel E., Robles, Mercedes, Andrade, Raul J., Montano-Loza, Aldo J., van den Brand, Floris F., Slooter, Charlotte D., Macedo, Guilherme, Liberal, Rodrigo, de Boer, Ynto S., and Lleo, Ana

Published
2024
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3. Incidence and predictors of hepatocellular carcinoma in patients with autoimmune hepatitis

Author

Colapietro, Francesca, primary, Maisonneuve, Patrick, additional, Lytvyak, Ellina, additional, Beuers, Ulrich, additional, Verdonk, Robert C., additional, van der Meer, Adriaan J., additional, van Hoek, Bart, additional, Kuiken, Sjoerd D., additional, Brouwer, Johannes T., additional, Muratori, Paolo, additional, Aghemo, Alessio, additional, Carella, Francesco, additional, van den Berg, Ad P., additional, Zachou, Kalliopi, additional, Dalekos, George N., additional, Di Zeo-Sánchez, Daniel E., additional, Robles, Mercedes, additional, Andrade, Raul J., additional, Montano-Loza, Aldo J., additional, van den Brand, Floris F., additional, Slooter, Charlotte D., additional, Macedo, Guilherme, additional, Liberal, Rodrigo, additional, de Boer, Ynto S., additional, Lleo, Ana, additional, van Gerven, N., additional, van Erpecum, K., additional, Ouden, J den, additional, Brouwer, J., additional, Vrolijk, J., additional, Gevers, T.J., additional, Drenth, J., additional, Guichelaar, M., additional, Bouma, G., additional, Schreuder, T.C.M.A., additional, van der Wouden, E.J., additional, Baak, L.C., additional, Stadhouders, P., additional, Klemt-Kropp, M., additional, Verhagen, M., additional, Bhalla, A., additional, Kuijvenhoven, J., additional, Almasio, P., additional, Alvarez, F., additional, Andrade, R., additional, Arikan, C., additional, Assis, D., additional, Bardou-Jacquet, E., additional, Biewenga, M., additional, Cancado, E., additional, Cazzagon, N., additional, Chazouillères, O., additional, Colloredo, G., additional, Cuarterolo, M., additional, Dalekos, G., additional, Debray, D., additional, Robles-Díaz, M., additional, Dyson, J., additional, Efe, C., additional, Engel, B., additional, Ferri, S., additional, Fontana, R., additional, Gatselis, N., additional, Gerussi, A., additional, Halilbasic, E., additional, Halliday, N., additional, Heneghan, M., additional, Hirschfield, G., additional, van Hoek, B., additional, Hørby Jørgensen, M., additional, Indolfini, G., additional, Iorio, R., additional, Invernizzi, P., additional, Jeong, S., additional, Jones, D., additional, Kelly, D., additional, Kerkar, N., additional, Lacaille, F., additional, Lammert, C., additional, Leggett, B., additional, Lenzi, M., additional, Levy, C., additional, Liberal, R., additional, Lleo, A., additional, Lohse, A., additional, Lopez, S. Ines, additional, de Martin, E., additional, McLin, V., additional, Mieli-Vergani, G., additional, Milkiewicz, P., additional, Mohan, N., additional, Muratori, L., additional, Nebbia, G., additional, van Nieuwkerk, C., additional, Oo, Y., additional, Ortega, A., additional, Páres, A., additional, Pop, T., additional, Pratt, D., additional, Purnak, T., additional, Ranucci, G., additional, Rushbrook, S., additional, Schramm, C., additional, Stättermayer, A., additional, Swain, M., additional, Tanaka, A., additional, Taubert, R., additional, Terrabuio, D., additional, Terziroli, B., additional, Trauner, M., additional, Valentino, P., additional, van den Brand, F., additional, Vergani, D., additional, Villamil, A., additional, Wahlin, S., additional, Ytting, H., additional, Zachou, K., additional, and Zeniya, M., additional

Published
2023
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4. Systematic review of response criteria and endpoints in autoimmune hepatitis by the International Autoimmune Hepatitis Group

Author

Pape, S, Snijders, R, Gevers, T, Chazouilleres, O, Dalekos, G, Hirschfield, G, Lenzi, M, Trauner, M, Manns, M, Vierling, J, Montano-Loza, A, Lohse, A, Schramm, C, Drenth, J, Heneghan, M, Almasio, P, Alvarez, F, Andrade, R, Arikan, C, Assis, D, Bardou-Jacquet, E, Biewenga, M, Cancado, E, Cazzagon, N, Colloredo, G, Cuarterolo, M, Debray, D, Robles-Diaz, M, Dyson, J, Efe, C, Engel, B, Ferri, S, Fontana, R, Gatselis, N, Gerussi, A, Halilbasic, E, Halliday, N, van Hoek, B, Horby Jorgensen, M, Indolfini, G, Iorio, R, Jeong, S, Jones, D, Kelly, D, Kerkar, N, Lacaille, F, Lammert, C, Leggett, B, Levy, C, Liberal, R, Lleo, A, Ines Lopez, S, de Martin, E, Mclin, V, Mieli-Vergani, G, Milkiewicz, P, Mohan, N, Muratori, L, Nebbia, G, van Nieuwkerk, C, Oo, Y, Ortega, A, Pares, A, Pop, T, Pratt, D, Purnak, T, Ranucci, G, Rushbrook, S, Stattermayer, A, Swain, M, Tanaka, A, Taubert, R, Terrabuio, D, Terziroli, B, Valentino, P, van den Brand, F, Villamil, A, Wahlin, S, Ytting, H, Zachou, K, Zeniya, M, Pape S., Snijders R. J. A. L. M., Gevers T. J. G., Chazouilleres O., Dalekos G. N., Hirschfield G. M., Lenzi M., Trauner M., Manns M. P., Vierling J. M., Montano-Loza A. J., Lohse A. W., Schramm C., Drenth J. P. H., Heneghan M. A., Almasio P., Alvarez F., Andrade R., Arikan C., Assis D., Bardou-Jacquet E., Biewenga M., Cancado E., Cazzagon N., Colloredo G., Cuarterolo M., Dalekos G., Debray D., Robles-Diaz M., Drenth J., Dyson J., Efe C., Engel B., Ferri S., Fontana R., Gatselis N., Gerussi A., Halilbasic E., Halliday N., Heneghan M., Hirschfield G., van Hoek B., Horby Jorgensen M., Indolfini G., Iorio R., Jeong S., Jones D., Kelly D., Kerkar N., Lacaille F., Lammert C., Leggett B., Levy C., Liberal R., Lleo A., Lohse A., Ines Lopez S., de Martin E., McLin V., Mieli-Vergani G., Milkiewicz P., Mohan N., Muratori L., Nebbia G., van Nieuwkerk C., Oo Y., Ortega A., Pares A., Pop T., Pratt D., Purnak T., Ranucci G., Rushbrook S., Stattermayer A., Swain M., Tanaka A., Taubert R., Terrabuio D., Terziroli B., Valentino P., van den Brand F., Villamil A., Wahlin S., Ytting H., Zachou K., Zeniya M., Pape, S, Snijders, R, Gevers, T, Chazouilleres, O, Dalekos, G, Hirschfield, G, Lenzi, M, Trauner, M, Manns, M, Vierling, J, Montano-Loza, A, Lohse, A, Schramm, C, Drenth, J, Heneghan, M, Almasio, P, Alvarez, F, Andrade, R, Arikan, C, Assis, D, Bardou-Jacquet, E, Biewenga, M, Cancado, E, Cazzagon, N, Colloredo, G, Cuarterolo, M, Debray, D, Robles-Diaz, M, Dyson, J, Efe, C, Engel, B, Ferri, S, Fontana, R, Gatselis, N, Gerussi, A, Halilbasic, E, Halliday, N, van Hoek, B, Horby Jorgensen, M, Indolfini, G, Iorio, R, Jeong, S, Jones, D, Kelly, D, Kerkar, N, Lacaille, F, Lammert, C, Leggett, B, Levy, C, Liberal, R, Lleo, A, Ines Lopez, S, de Martin, E, Mclin, V, Mieli-Vergani, G, Milkiewicz, P, Mohan, N, Muratori, L, Nebbia, G, van Nieuwkerk, C, Oo, Y, Ortega, A, Pares, A, Pop, T, Pratt, D, Purnak, T, Ranucci, G, Rushbrook, S, Stattermayer, A, Swain, M, Tanaka, A, Taubert, R, Terrabuio, D, Terziroli, B, Valentino, P, van den Brand, F, Villamil, A, Wahlin, S, Ytting, H, Zachou, K, Zeniya, M, Pape S., Snijders R. J. A. L. M., Gevers T. J. G., Chazouilleres O., Dalekos G. N., Hirschfield G. M., Lenzi M., Trauner M., Manns M. P., Vierling J. M., Montano-Loza A. J., Lohse A. W., Schramm C., Drenth J. P. H., Heneghan M. A., Almasio P., Alvarez F., Andrade R., Arikan C., Assis D., Bardou-Jacquet E., Biewenga M., Cancado E., Cazzagon N., Colloredo G., Cuarterolo M., Dalekos G., Debray D., Robles-Diaz M., Drenth J., Dyson J., Efe C., Engel B., Ferri S., Fontana R., Gatselis N., Gerussi A., Halilbasic E., Halliday N., Heneghan M., Hirschfield G., van Hoek B., Horby Jorgensen M., Indolfini G., Iorio R., Jeong S., Jones D., Kelly D., Kerkar N., Lacaille F., Lammert C., Leggett B., Levy C., Liberal R., Lleo A., Lohse A., Ines Lopez S., de Martin E., McLin V., Mieli-Vergani G., Milkiewicz P., Mohan N., Muratori L., Nebbia G., van Nieuwkerk C., Oo Y., Ortega A., Pares A., Pop T., Pratt D., Purnak T., Ranucci G., Rushbrook S., Stattermayer A., Swain M., Tanaka A., Taubert R., Terrabuio D., Terziroli B., Valentino P., van den Brand F., Villamil A., Wahlin S., Ytting H., Zachou K., and Zeniya M.

Abstract

Background & Aims: Autoimmune hepatitis (AIH) has been well characterised and codified through the development of diagnostic criteria. These criteria have been adapted and simplified and are widely used in clinical practice. However, there is a need to update and precisely define the criteria for both treatment response and treatment. Methods: A systematic review was performed and a modified Delphi consensus process was used to identify and redefine the response criteria in autoimmune hepatitis. Results: The consensus process initiated by the International Autoimmune Hepatitis Group proposes that the term ‘complete biochemical response’ defined as ‘normalization of serum transaminases and IgG below the upper limit of normal’ be adopted to include a time point at 6 months after initiation of treatment. An insufficient response by 6 months was a failure to meet the above definition. Non-response was defined as ‘<50% decrease of serum transaminases within 4 weeks after initiation of treatment’. Remission is defined as liver histology with a Hepatitis Activity Index <4/18. Intolerance to treatment was agreed to stand for ‘any adverse event possibly related to treatment leading to potential drug discontinuation’. Conclusions: These definitions provide a simple and reproducible framework to define treatment response and non-response, irrespective of the therapeutic intervention. A consensus on endpoints is urgently required to set a global standard for the reporting of study results and to enable inter-study comparisons. Future prospective database studies are needed to validate these endpoints. Lay summary: Consensus among international experts on response criteria and endpoints in autoimmune hepatitis is lacking. A consensus on endpoints is urgently required to set a global standard for the reporting of study results and to enable the comparison of results between clinical trials. Therefore, the International Autoimmune Hepatitis Group (IAIHG) herein presents

Published
2022

6. Systematic review of response criteria and endpoints in autoimmune hepatitis by the International Autoimmune Hepatitis Group

Author

Pape, Simon, primary, Snijders, Romée J.A.L.M., additional, Gevers, Tom J.G., additional, Chazouilleres, Oliver, additional, Dalekos, George N., additional, Hirschfield, Gideon M., additional, Lenzi, Marco, additional, Trauner, Michael, additional, Manns, Michael P., additional, Vierling, John M., additional, Montano-Loza, Aldo J., additional, Lohse, Ansgar W., additional, Schramm, Christoph, additional, Drenth, Joost P.H., additional, Heneghan, Michael A., additional, Almasio, P., additional, Alvarez, F., additional, Andrade, R., additional, Arikan, C., additional, Assis, D., additional, Bardou-Jacquet, E., additional, Biewenga, M., additional, Cancado, E., additional, Cazzagon, N., additional, Chazouillères, O., additional, Colloredo, G., additional, Cuarterolo, M., additional, Dalekos, G., additional, Debray, D., additional, Robles-Díaz, M., additional, Drenth, J., additional, Dyson, J., additional, Efe, C., additional, Engel, B., additional, Ferri, S., additional, Fontana, R., additional, Gatselis, N., additional, Gerussi, A., additional, Halilbasic, E., additional, Halliday, N., additional, Heneghan, M., additional, Hirschfield, G., additional, van Hoek, B., additional, Hørby Jørgensen, M., additional, Indolfini, G., additional, Iorio, R., additional, Jeong, S., additional, Jones, D., additional, Kelly, D., additional, Kerkar, N., additional, Lacaille, F., additional, Lammert, C., additional, Leggett, B., additional, Lenzi, M., additional, Levy, C., additional, Liberal, R., additional, Lleo, A., additional, Lohse, A., additional, Ines Lopez, S., additional, de Martin, E., additional, McLin, V., additional, Mieli-Vergani, G., additional, Milkiewicz, P., additional, Mohan, N., additional, Muratori, L., additional, Nebbia, G., additional, van Nieuwkerk, C., additional, Oo, Y., additional, Ortega, A., additional, Páres, A., additional, Pop, T., additional, Pratt, D., additional, Purnak, T., additional, Ranucci, G., additional, Rushbrook, S., additional, Schramm, C., additional, Stättermayer, A., additional, Swain, M., additional, Tanaka, A., additional, Taubert, R., additional, Terrabuio, D., additional, Terziroli, B., additional, Trauner, M., additional, Valentino, P., additional, van den Brand, F., additional, Villamil, A., additional, Wahlin, S., additional, Ytting, H., additional, Zachou, K., additional, and Zeniya, M., additional

Published
2022
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7. P409 FMT induced increase in gut microbial diversity and Clostridia is associated with clinical response in patients with ulcerative colitis – results from STOP Colitis trial

Author

Quraishi, M N, primary, Quince, C, additional, Hewitt, C, additional, Beggs, A, additional, Gerasimidis, K, additional, Sharma, N, additional, Hawkey, P, additional, Oo, Y, additional, Ives, N, additional, Manzoor, S, additional, Loman, N, additional, Hansen, R, additional, Hart, A, additional, Gaya, D, additional, and Iqbal, T, additional

Published
2022
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10. Immune system and cholangiocytes: A puzzling affair in primary biliary cholangitis

Author

Ronca, V, Mancuso, C, Milani, C, Carbone, M, Oo, Y, Invernizzi, P, Oo, YH, Ronca, V, Mancuso, C, Milani, C, Carbone, M, Oo, Y, Invernizzi, P, and Oo, YH

Abstract

Primary biliary cholangitis (PBC) is a cholestatic liver disease characterized by the destruction of the small and medium bile ducts. Its pathogenesis is still unknown. Despite the genome wide association study findings, the therapies targeting the cytokines pathway, tested so far, have failed. The concept of the biliary epithelium as a key player of the PBC pathogenesis has emerged over the last few years. It is now well accepted that the biliary epithelial cells (BECs) actively participate to the genesis of the damage. The chronic stimulation of BECs via microbes and bile changes the cell phenotype toward an active state, which, across the production of proinflammatory mediators, can recruit, retain, and activate immune cells. The consequent immune system activation can in turn damage BECs. Thus, the crosstalk between both innate and adaptive immune cells and the biliary epithelium creates a paracrine loop responsible for the disease progression. In this review, we summarize the evidence provided in literature about the role of BECs and the immune system in the pathogenesis of PBC. We also dissect the relationship between the immune system and the BECs, focusing on the unanswered questions and the future potential directions of the translational research and the cellular therapy in this area.

Published
2020

12. OP09 Immunomodulatory mechanisms of faecal microbiota transplantation are associated with clinical response in ulcerative colitis: early results from STOP-Colitis

Author

Quraishi, M N, primary, Oo, Y H, additional, Beggs, A, additional, Withers, D, additional, Acharjee, A, additional, Sharma, N, additional, Manzoor, S, additional, Hart, A L, additional, Gaya, D R, additional, Loman, N J, additional, Hawkey, P M, additional, Gerasimidis, K, additional, Hansen, R, additional, Gkoutous, G, additional, and Iqbal, T H, additional

Published
2020
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13. Low‐dose interleukin‐2 promotes STAT‐5 phosphorylation, Treg survival and CTLA‐4‐dependent function in autoimmune liver diseases

Author

Jeffery, H. C., Jeffery, L. E., Lutz, P., Corrigan, M., Webb, G. J., Hirschfield, G. M., Adams, D. H., and Oo, Y. H.

Subjects
Adult, Male, chemical and pharmacologic phenomena, Autoimmunity, T-Lymphocytes, Regulatory, regulatory T cells, Autoimmune Diseases, Young Adult, STAT5 Transcription Factor, Humans, CTLA-4 Antigen, Phosphorylation, Cells, Cultured, Aged, CTLA‐4, Liver Diseases, Translational, autoimmune liver disease, Bcl‐2, hemic and immune systems, Original Articles, Middle Aged, Flow Cytometry, Recombinant Proteins, interleukin‐2, Case-Control Studies, Interleukin-2, Original Article, STAT‐5, Female, Biomarkers
Abstract

Summary CD4+CD25highCD127lowforkhead box protein 3 (FoxP3+) regulatory T cells (Treg) are essential for the maintenance of peripheral tolerance. Impaired Treg function and an imbalance between effector and Tregs contribute to the pathogenesis of autoimmune diseases. We reported recently that the hepatic microenvironment is deficient in interleukin (IL)−2, a cytokine essential for Treg survival and function. Consequently, few liver‐infiltrating Treg demonstrate signal transducer and activator of transcription‐5 (STAT‐5) phosphorylation. To establish the potential of IL‐2 to enhance Treg therapy, we investigated the effects of very low dose Proleukin (VLDP) on the phosphorylation of STAT‐5 and the subsequent survival and function of Treg and T effector cells from the blood and livers of patients with autoimmune liver diseases. VLDP, at less than 5 IU/ml, resulted in selective phosphorylation of STAT‐5 in Treg but not effector T cells or natural killer cells and associated with increased expression of cytotoxic T lymphocyte antigen‐4 (CTLA‐4), FoxP3 and CD25 and the anti‐apoptotic protein Bcl‐2 in Treg with the greatest enhancement of regulatory phenotype in the effector memory Treg population. VLDP also maintained expression of the liver‐homing chemokine receptor CXCR3. VLDP enhanced Treg function in a CTLA‐4‐dependent manner. These findings open new avenues for future VLDP cytokine therapy alone or in combination with clinical grade Treg in autoimmune liver diseases, as VLDP could not only enhance regulatory phenotype and functional property but also the survival of intrahepatic Treg.

Published
2017

18. P2.04-86 Efficacy of Ipilimumab in Combination with Chemotherapy for First-Line Treatment of Advanced Lung Cancer

Author

Htut, T., primary, Tun, A., additional, Swarup, S., additional, Sultan, A., additional, Mogollon-Duffo, F., additional, Jahan, N., additional, Adhikari, N., additional, Oo, Y., additional, Thida, A., additional, Aung, H., additional, Thi, W., additional, Panigrahi, K., additional, Tijani, L., additional, and Thein, K., additional

Published
2019
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19. Chronic Hepatitis C Virus infection subverts vaccine induced T-cell immunity in humans

Author

Kelly, C, Swadling, L, Capone, S, Brown, A, Richardson, R, Halliday, J, von Delft, A, Oo, Y, Mutimer, D, Kurioka, A, Hartnell, F, Collier, J, Ammendola, V, Del Sorbo, M, Grazioli, F, Luisa Esposito, M, Di Marco, S, Siani, L, Traboni, C, Hill, A, Colloca, S, Nicosia, A, Cortese, R, Folgori, A, Klenerman, P, Barnes, E, Kelly, C, Swadling, L, Capone, S, Brown, A, Richardson, R, Halliday, J, von Delft, A, Oo, Y, Mutimer, D, Kurioka, A, Hartnell, F, Collier, J, Ammendola, V, Del Sorbo, M, Grazioli, F, Esposito, Ml, Di Marco, S, Siani, L, Traboni, C, Hill, Av, Colloca, S, Nicosia, A, Cortese, R, Folgori, A, Klenerman, P, and Barnes, E

Abstract

Adenoviral vectors encoding hepatitis C virus (HCV) nonstructural (NS) proteins induce multispecific, high-magnitude, durable CD4(+) and CD8(+) T-cell responses in healthy volunteers. We assessed the capacity of these vaccines to induce functional HCV-specific immune responses and determine T-cell cross-reactivity to endogenous virus in patients with chronic HCV infection. HCV genotype 1-infected patients were vaccinated using heterologous adenoviral vectors (ChAd3-NSmut and Ad6-NSmut) encoding HCV NS proteins in a dose escalation, prime-boost regimen, with and without concomitant pegylated interferon-α/ribavirin therapy. Analysis of immune responses ex vivo used human leukocyte antigen class I pentamers, intracellular cytokine staining, and fine mapping in interferon-γ enzyme-linked immunospot assays. Cross-reactivity of T cells with population and endogenous viral variants was determined following viral sequence analysis. Compared to healthy volunteers, the magnitude of HCV-specific T-cell responses following vaccination was markedly reduced. CD8(+) HCV-specific T-cell responses were detected in 15/24 patients at the highest dose, whereas CD4(+) T-cell responses were rarely detectable. Analysis of the host circulating viral sequence showed that T-cell responses were rarely elicited when there was sequence homology between vaccine immunogen and endogenous virus. In contrast, T cells were induced in the context of genetic mismatch between vaccine immunogen and endogenous virus; however, these commonly failed to recognize circulating epitope variants and had a distinct partially functional phenotype. Vaccination was well tolerated but had no significant effect on HCV viral load. CONCLUSION: Vaccination with potent HCV adenoviral vectored vaccines fails to restore T-cell immunity except where there is genetic mismatch between vaccine immunogen and endogenous virus; this highlights the major challenge of overcoming T-cell exhaustion in the context of persistent antigen exposure with implications for cancer and other persistent infections.

Published
2016

20. Chronic hepatitis C viral infection subverts vaccine-induced T-cell immunity in humans

Author

Kelly, C, Swadling, L, Capone, S, Brown, A, Richardson, R, Halliday, J, von Delft, A, Oo, Y, Mutimer, D, Kurioka, A, Hartnell, F, Collier, J, Ammendola, V, Sorbo, MD, Grazioli, F, Esposito, ML, Marco, SD, Siani, L, Traboni, C, Hill, A, Colloca, S, Nicosia, A, Cortese, R, Folgori, A, Klenerman, P, and Barnes, E

Abstract

Adenoviral vectors encoding hepatitis C virus (HCV) nonstructural (NS) proteins induce multispecific, high-magnitude, durable CD4+ and CD8+ T-cell responses in healthy volunteers. We assessed the capacity of these vaccines to induce functional HCV-specific immune responses and determine T-cell cross-reactivity to endogenous virus in patients with chronic HCV infection. HCV genotype 1-infected patients were vaccinated using heterologous adenoviral vectors (ChAd3-NSmut and Ad6-NSmut) encoding HCV NS proteins in a dose escalation, prime-boost regimen, with and without concomitant pegylated interferon-α/ribavirin therapy. Analysis of immune responses ex vivo used human leukocyte antigen class I pentamers, intracellular cytokine staining, and fine mapping in interferon-γ enzyme-linked immunospot assays. Cross-reactivity of T cells with population and endogenous viral variants was determined following viral sequence analysis. Compared to healthy volunteers, the magnitude of HCV-specific T-cell responses following vaccination was markedly reduced. CD8+ HCV-specific T-cell responses were detected in 15/24 patients at the highest dose, whereas CD4+ T-cell responses were rarely detectable. Analysis of the host circulating viral sequence showed that T-cell responses were rarely elicited when there was sequence homology between vaccine immunogen and endogenous virus. In contrast, T cells were induced in the context of genetic mismatch between vaccine immunogen and endogenous virus; however, these commonly failed to recognize circulating epitope variants and had a distinct partially functional phenotype. Vaccination was well tolerated but had no significant effect on HCV viral load. Conclusion: Vaccination with potent HCV adenoviral vectored vaccines fails to restore T-cell immunity except where there is genetic mismatch between vaccine immunogen and endogenous virus; this highlights the major challenge of overcoming T-cell exhaustion in the context of persistent antigen exposure with implications for cancer and other persistent infections.

Published
2017

22. Immunological mechanisms underpinning faecal microbiota transplantation for the treatment of inflammatory bowel disease.

Author

Quraishi, M. N., Shaheen, W., Oo, Y. H., and Iqbal, T. H.

Subjects
INFLAMMATORY bowel diseases, TRANSPLANTATION of organs, tissues, etc., GUT microbiome, GASTROINTESTINAL diseases, COMMUNITY change
Abstract

Summary: Inflammatory bowel disease (IBD) is a chronic gastrointestinal disease that results from a dysregulated immune response against specific environmental triggers in a genetically predisposed individual. Increasing evidence has indicated a causal role for changes in gut microbiota (dysbiosis) contributing to this immune‐mediated intestinal inflammation. These mechanisms involve dysregulation of multiple facets of the host immune pathways that are potentially reversible. Faecal microbiota transplantation (FMT) is the transfer of processed stool from a healthy donor into an individual with an illness. FMT has shown promising results in both animal model experiments and clinical studies in IBD in the resolution of intestinal inflammation. The underlying mechanisms, however, are unclear. Insights from these studies have shown interactions between modulation of dysbiosis via changes in abundances of specific members of the gut microbial community and changes in host immunological pathways. Unravelling these causal relationships has promising potential for a translational therapy role to develop targeted microbial therapies and understand the mechanisms that underpin IBD aetiopathogenesis. In this review, we discuss current evidence for the contribution of gut microbiota in the disruption of intestinal immune homeostasis and immunoregulatory mechanisms that are associated with the resolution of inflammation through FMT in IBD. [ABSTRACT FROM AUTHOR]

Published
2020
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25. Autoimmune hepatitis with normal IgG at diagnosis: Subtype without selective elevation of IgG but similar histological features and treatment response

Author

Hartl, J, additional, Wong, G, additional, Zachou, K, additional, Ashgar, A, additional, Pape, S, additional, Sebode, M, additional, Peiseler, M, additional, Weiler-Normann, C, additional, Zenouzi, R, additional, Krech, T, additional, Ehlken, H, additional, Huebscher, S, additional, Miquel, R, additional, Schramm, C, additional, Drenth, J, additional, Oo, Y, additional, Dalekos, G, additional, Heneghan, M, additional, and Lohse, A, additional

Published
2018
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26. Flares during long-term entecavir therapy in chronic hepatitis B

Author

Chi, Heng, Arends, Pauline, Reijnders, Jurriën, Carey, I, Brown, A, Fasano, M, Mutimer, D, Deterding, K, Oo, Y H, Petersen, J, van Bommel, F, de Knegt, Rob, Santantonio, T A, Berg, T, Welzel, TM, Wedemeyer, H, Buti, M, Pradat, P, Zoulim, F, Hansen, Bettina, Janssen, HLA, Forest Research, Alice Holt Lodge, Medcom [Odense], Norwegian Institute for Air Research (NILU), Norwegian University of Science and Technology [Trondheim] (NTNU), Norwegian University of Science and Technology (NTNU), Equipe 16, Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherche en Cancérologie de Lyon (CRCL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and Gastroenterology & Hepatology

Subjects
Adult, Male, Canada, Hepatitis B virus, Guanine, Biomedical Research, Patients, Drug Resistance, [SDV.CAN]Life Sciences [q-bio]/Cancer, Antiviral Agents, methods, Hepatitis, Hepatitis B, Chronic, Endocrinology, SDG 3 - Good Health and Well-being, Germany, London, Humans, Hepatitis B e Antigens, therapy, Hepatitis B Surface Antigens, Incidence, Gastroenterology, Alanine Transaminase, Middle Aged, Hepatitis B, Liver, Italy, DNA, Viral, Female, France, Biomarkers, Follow-Up Studies
Abstract

International audience; BACKGROUND AND AIM: The incidence and consequences of flares during first-line nucleos(t)ide analogue therapy are largely unknown. We aimed to investigate the incidence and outcome of alanine aminotransferase (ALT) flares during long-term entecavir (ETV) in chronic hepatitis B (CHB). METHODS: CHB patients treated with ETV monotherapy from 11 European centers were studied. Flare was defined as \textgreater 3x increase in ALT compared with baseline or lowest on-treatment level and an absolute ALT \textgreater 3x ULN. Flares were designated as host-induced (preceded by hepatitis B virus (HBV)-DNA decline), virus-induced (HBV-DNA increase), or indeterminate (stable HBV-DNA). RESULTS: Seven hundred and twenty-nine patients were treated with ETV for median of 3.5 years. Thirty patients developed a flare with cumulative incidence of 6.3% at year 5. Baseline hepatitis B e antigen (HBeAg)-positivity (HR 2.84; P = 0.005) and high HBV-DNA (Hazard ratio (HR) 1.30; P = 0.003) predicted flares. There were 12 (40%) host-induced, 7 (23%) virus-induced, and 11 (37%) indeterminate flares. Host-induced flares occurred earlier than virus-induced (median: 15 vs 83 weeks; P = 0.027) or indeterminate flares (15 vs 109 weeks; P = 0.011). Host-induced flares were associated with biochemical remission, and HBeAg (n = 3) and hepatitis B surface antigen (n = 2) seroconversions were exclusively observed among patients with these flares. Virus-induced flares were associated with ETV resistance (n = 2) and non-compliance (n = 1). CONCLUSION: The incidence of ALT flares during ETV was low in this real-life cohort. ETV can be safely continued in patients with host-induced flares. Treatment adherence and drug resistance must be assessed in patients with virus-induced flares

Published
2016

27. Hepatitis Hide and Seek

Author

Barnes, E, Folgori, A, Capone, S, Swadling, L, Aston, S, Kurioka, A, Meyer, J, Huddart, R, Smith, K, Townsend, R, Brown, A, Antrobus, R, Ammendola, V, Naddeo, M, O'Hara, G, Willberg, C, Harrison, A, Grazioli, F, Esposito, M, Siani, L, Traboni, C, Oo, Y, Adams, D, Hill, A, and Colloca, S

Published
2016

31. The ACCURE-UK trial: The effect of appendectomy on the clinical course of ulcerative colitis – A feasibility study

Author

Nepogodiev, D., primary, Howard, R., additional, Pathmakanthan, S., additional, Iqbal, T., additional, Singh, B., additional, Oo, Y., additional, Mathers, J., additional, McMullan, C., additional, Sahamai, S., additional, Gath, J., additional, Magill, L., additional, Handley, K., additional, Deeks, J., additional, Bemelman, W., additional, Morton, D., additional, and Pinkney, T., additional

Published
2016
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32. Hepatitis Hide and Seek

Author

Barnes, E, Folgori, A, Capone, S, Swadling, L, Aston, S, Kurioka, A, Meyer, J, Huddart, R, Smith, K, Townsend, R, Brown, A, Antrobus, R, Ammendola, V, Naddeo, M, O'Hara, G, Willberg, C, Harrison, A, Grazioli, F, Esposito, ML, Siani, L, Traboni, C, Oo, Y, Adams, D, Hill, A, Colloca, S, Nicosia, A, Cortese, R, and Klenerman, P

Published
2012

34. P0661 : Prediction of HBeAg seroconversion in HBeAg-positive chronic hepatitis B patients treated with entecavir using ALT and platelet count: Results from a large european multi-center study

Author

Chi, H., primary, van Bömmel, F., additional, Buti, M., additional, Brown, A., additional, Carey, I., additional, Fasano, M., additional, Mutimer, D., additional, Deterding, K., additional, Oo, Y., additional, Arends, P., additional, de Knegt, R.J., additional, Santantonio, T., additional, Welzel, T.M., additional, Pradat, P., additional, Petersen, J., additional, Wedemeyer, H., additional, Berg, T., additional, Zoulim, F., additional, Hansen, B.E., additional, and Janssen, H.L, additional

Published
2015
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36. Low-dose interleukin-2 promotes STAT-5 phosphorylation, Treg survival and CTLA-4-dependent function in autoimmune liver diseases.

Author

Jeffery, H. C., Jeffery, L. E., Lutz, P., Corrigan, M., Webb, G. J., Hirschfield, G. M., Adams, D. H., and Oo, Y. H.

Subjects
LIVER diseases, LIVER disease treatment, AUTOIMMUNE diseases, INTERLEUKIN-2, STAT proteins, PHOSPHORYLATION, IMMUNOLOGY
Abstract

CD4+CD25highCD127lowforkhead box protein 3 (FoxP3+) regulatory T cells (Treg) are essential for the maintenance of peripheral tolerance. Impaired Treg function and an imbalance between effector and Tregs contribute to the pathogenesis of autoimmune diseases. We reported recently that the hepatic microenvironment is deficient in interleukin (IL)−2, a cytokine essential for Treg survival and function. Consequently, few liver-infiltrating Treg demonstrate signal transducer and activator of transcription-5 (STAT-5) phosphorylation. To establish the potential of IL-2 to enhance Treg therapy, we investigated the effects of very low dose Proleukin (VLDP) on the phosphorylation of STAT-5 and the subsequent survival and function of Treg and T effector cells from the blood and livers of patients with autoimmune liver diseases. VLDP, at less than 5 IU/ml, resulted in selective phosphorylation of STAT-5 in Treg but not effector T cells or natural killer cells and associated with increased expression of cytotoxic T lymphocyte antigen-4 (CTLA-4), FoxP3 and CD25 and the anti-apoptotic protein Bcl-2 in Treg with the greatest enhancement of regulatory phenotype in the effector memory Treg population. VLDP also maintained expression of the liver-homing chemokine receptor CXCR3. VLDP enhanced Treg function in a CTLA-4-dependent manner. These findings open new avenues for future VLDP cytokine therapy alone or in combination with clinical grade Treg in autoimmune liver diseases, as VLDP could not only enhance regulatory phenotype and functional property but also the survival of intrahepatic Treg. [ABSTRACT FROM AUTHOR]

Published
2017
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37. Osteopontin neutralisation abrogates the liver progenitor cell response and fibrogenesis in mice

Author

Coombes, J D, primary, Swiderska-Syn, M, additional, Dollé, L, additional, Reid, D, additional, Eksteen, B, additional, Claridge, L, additional, Briones-Orta, M A, additional, Shetty, S, additional, Oo, Y H, additional, Riva, A, additional, Chokshi, S, additional, Papa, S, additional, Mi, Z, additional, Kuo, P C, additional, Williams, R, additional, Canbay, A, additional, Adams, D H, additional, Diehl, A M, additional, van Grunsven, L A, additional, Choi, S S, additional, and Syn, W K, additional

Published
2014
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38. Pheochromocytoma: A review

Author

Tsirlin, A., primary, Oo, Y., additional, Sharma, R., additional, Kansara, A., additional, Gliwa, A., additional, and Banerji, M.A., additional

Published
2014
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41. High-resolution96Zr(3He,t) experiment and the matrix element for double-βdecay

Author

Thies, J. H., primary, Puppe, P., additional, Adachi, T., additional, Dozono, M., additional, Ejiri, H., additional, Frekers, D., additional, Fujita, H., additional, Fujita, Y., additional, Fujiwara, M., additional, Grewe, E.-W., additional, Hatanaka, K., additional, Heinrichs, P., additional, Ishikawa, D., additional, Khai, N. T., additional, Lennarz, A., additional, Matsubara, H., additional, Okamura, H., additional, Oo, Y. Y., additional, Ruhe, T., additional, Suda, K., additional, Tamii, A., additional, Yoshida, H. P., additional, and Zegers, R. G. T., additional

Published
2012
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42. High-resolution100Mo(3He,t)100Tc charge-exchange experiment and the impact on double-βdecays and neutrino charged-current reactions

Author

Thies, J. H., primary, Adachi, T., additional, Dozono, M., additional, Ejiri, H., additional, Frekers, D., additional, Fujita, H., additional, Fujita, Y., additional, Fujiwara, M., additional, Grewe, E.-W., additional, Hatanaka, K., additional, Heinrichs, P., additional, Ishikawa, D., additional, Khai, N. T., additional, Lennarz, A., additional, Matsubara, H., additional, Okamura, H., additional, Oo, Y. Y., additional, Puppe, P., additional, Ruhe, T., additional, Suda, K., additional, Tamii, A., additional, Yoshida, H. P., additional, and Zegers, R. G. T., additional

Published
2012
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43. The (3He,t) reaction on76Ge, and the double-β-decay matrix element

Author

Thies, J. H., primary, Frekers, D., additional, Adachi, T., additional, Dozono, M., additional, Ejiri, H., additional, Fujita, H., additional, Fujita, Y., additional, Fujiwara, M., additional, Grewe, E.-W., additional, Hatanaka, K., additional, Heinrichs, P., additional, Ishikawa, D., additional, Khai, N. T., additional, Lennarz, A., additional, Matsubara, H., additional, Okamura, H., additional, Oo, Y. Y., additional, Puppe, P., additional, Ruhe, T., additional, Suda, K., additional, Tamii, A., additional, Yoshida, H. P., additional, and Zegers, R. G. T., additional

Published
2012
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