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Journal articles on the topic 'Liver disease; Immunology'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 February 2022

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1

Leevy, Carroll B., and Hany A. Elbeshbeshy. "Immunology of Alcoholic Liver Disease." Clinics in Liver Disease 9, no. 1 (February 2005): 55–66. http://dx.doi.org/10.1016/j.cld.2004.11.002.

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2

Duddempudi, Anupama T. "Immunology in Alcoholic Liver Disease." Clinics in Liver Disease 16, no. 4 (November 2012): 687–98. http://dx.doi.org/10.1016/j.cld.2012.08.003.

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3

Chedid, Antonio, Selma Arain, Ann Snyder, Philippe Mathurin, Frédérique Capron, and Sylvie Naveau. "The Immunology of Fibrogenesis in Alcoholic Liver Disease." Archives of Pathology & Laboratory Medicine 128, no. 11 (November 1, 2004): 1230–38. http://dx.doi.org/10.5858/2004-128-1230-tiofia.

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Abstract Context.—Alcoholic liver disease in humans frequently leads to cirrhosis. Experimental models of hepatic fibrogenesis are available, but extrapolation of those findings to human ethanol-induced liver injury is difficult. Hepatic ethanol-induced fibrosis in humans has often been studied in relatively small patient populations. During the past decade, several animal models and human studies have attributed fibrogenesis in the liver to the role played by hepatocytes, Kupffer cells, endothelial cells, and especially stellate cells. Objective.—To determine the contribution of the main liver cell types to ethanol-induced fibrogenesis. For that purpose, we studied the expression of the following immunologic parameters: smooth muscle–specific α actin (SMSA), CD68, CD34, transforming growth factor β1, intercellular adhesion molecule 1, and collagen types 1 and 3. The Dako LSAB+ kit (peroxidase method) was used. Design.—We recently studied a large cohort of patients with alcoholic liver disease in France. In this cohort, we found 87 cases in which liver biopsies revealed only pericentral injury with nonpathologic portal areas. We compared cases in which the portal areas were nonpathologic with 324 patients in whom staging ranged from F0 to F3. Patients with cirrhosis (F4) were excluded from evaluation. To stage fibrosis, we used the METAVIR system. Furthermore, we selected 40 cases in which the biopsies measured at least 25 mm in length for further histochemical evaluation. Ten additional normal cases from our archives were used as controls. We divided this patient population into the following 5 groups of 10 patients each: group 1A, F0 with steatosis; group 1B, F0 without steatosis; group 2, F0 to F1, central injury; group 3, F3, fibrosis with multiple septa; and group 4, nonpathologic livers (controls). Results.—Smooth muscle–specific α actin was expressed by stellate cells, pericentrally, with increasing severity and intensity in the advanced stage of fibrosis of group 3, less intense expression was noted in group 2, and expression was practically absent in group 1 and in nonpathologic controls. CD68 was the best marker for Kupffer cells and was expressed diffusely within the lobules in all groups. Its expression correlated directly with the degree of disease severity, progressing from stage I through stage III, but was absent in nonpathologic livers. CD34 was consistently expressed by endothelial cells in the periportal areas in all groups. The expression of collagen type 1 was intense in the bands of fibrosis or bridging, while type 3 expression was poor. Transforming growth factor β1 and intercellular adhesion molecule 1 were not expressed in any group. Conclusions.—In this study, stellate cell activation (SMSA) was most intense pericentrally in the early stages and diffusely with progression to fibrosis and maximum intensity in stage III. Kupffer cell activation, as determined by CD68 expression, was intense and diffuse, while endothelial cells expressed CD34 periportally in a similar manner in all stages. Fibrogenesis in human ethanol injury is due to the activity of stellate cells, Kupffer cells, and to a lesser extent, to endothelial cells.
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4

Mutchnick, Milton G. "Immunology of liver disease. Seminars in liver disease, vol. 4, number 1." Gastroenterology 89, no. 4 (October 1985): 923–24. http://dx.doi.org/10.1016/0016-5085(85)90598-0.

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5

Bejarano, P. A. "The Immunology of Fibrogenesis in Alcoholic Liver Disease." Yearbook of Pathology and Laboratory Medicine 2006 (January 2006): 30–31. http://dx.doi.org/10.1016/s1077-9108(08)70025-2.

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6

Heymann, Felix, and Frank Tacke. "Immunology in the liver — from homeostasis to disease." Nature Reviews Gastroenterology & Hepatology 13, no. 2 (January 13, 2016): 88–110. http://dx.doi.org/10.1038/nrgastro.2015.200.

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7

Neuberger, James, and Roger Williams. "12 Immunology of drug and alcohol-induced liver disease." Baillière's Clinical Gastroenterology 1, no. 3 (July 1987): 707–22. http://dx.doi.org/10.1016/0950-3528(87)90054-6.

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8

TODA, GOTARO. "Immunology on the digestive system.5.Disease state of autoimmune liver diseases." Nihon Naika Gakkai Zasshi 82, no. 9 (1993): 1403–8. http://dx.doi.org/10.2169/naika.82.1403.

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9

Utiyama, Shirley R. R., Katiane B. Zenatti, Heloisa A. J. Nóbrega, Juliana Z. C. Soares, Thelma L. Skare, Caroline Matsubara, Dominique A. Muzzilo, and Renato M. Nisihara. "Rheumatic Disease Autoantibodies in Autoimmune Liver Diseases." Immunological Investigations 45, no. 6 (July 13, 2016): 566–73. http://dx.doi.org/10.1080/08820139.2016.1186173.

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10

Schimpf, Kl. "Liver disease in hemophilia." Transfusion Science 11 (January 1990): S15—S22. http://dx.doi.org/10.1016/0955-3886(90)90078-w.

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11

Ma, Bingquan, Peng Li, Hengyuan An, and Zhiming Song. "Electroacupuncture Attenuates Liver Inflammation in Nonalcoholic Fatty Liver Disease Rats." Inflammation 43, no. 6 (July 31, 2020): 2372–78. http://dx.doi.org/10.1007/s10753-020-01306-w.

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12

Morse, Caryn G. "Fatty liver disease in HIV." AIDS 31, no. 11 (July 2017): 1633–35. http://dx.doi.org/10.1097/qad.0000000000001525.

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13

Highton, A. J., I. S. Schuster, M. A. Degli-Esposti, and M. Altfeld. "The role of natural killer cells in liver inflammation." Seminars in Immunopathology 43, no. 4 (July 7, 2021): 519–33. http://dx.doi.org/10.1007/s00281-021-00877-6.

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AbstractThe liver is an important immunological site that can promote immune tolerance or activation. Natural killer (NK) cells are a major immune subset within the liver, and therefore understanding their role in liver homeostasis and inflammation is crucial. Due to their cytotoxic function, NK cells are important in the immune response against hepatotropic viral infections but are also involved in the inflammatory processes of autoimmune liver diseases and fatty liver disease. Whether NK cells primarily promote pro-inflammatory or tolerogenic responses is not known for many liver diseases. Understanding the involvement of NK cells in liver inflammation will be crucial in effective treatment and future immunotherapeutic targeting of NK cells in these disease settings. Here, we explore the role that NK cells play in inflammation of the liver in the context of viral infection, autoimmunity and fatty liver disease.
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14

Muratori, L., P. Muratori, D. Zauli, A. Grassi, G. Pappas, L. Rodrigo, F. Cassani, M. Lenzi, and F. B. Bianchi. "Antilactoferrin antibodies in autoimmune liver disease." Clinical & Experimental Immunology 124, no. 3 (June 2001): 470–73. http://dx.doi.org/10.1046/j.1365-2249.2001.01524.x.

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15

Ishibashi, Hiromi, Minoru Nakamura, Atsumasa Komori, Kiyoshi Migita, and Shinji Shimoda. "Liver architecture, cell function, and disease." Seminars in Immunopathology 31, no. 3 (May 26, 2009): 399–409. http://dx.doi.org/10.1007/s00281-009-0155-6.

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16

Freeman, Richard B., Ann Harper, and Erick B. Edwards. "Liver transplantation outcomes under the model for end-stage liver disease and pediatric end-stage liver disease." Current Opinion in Organ Transplantation 10, no. 2 (June 2005): 90–94. http://dx.doi.org/10.1097/01.mot.0000161760.02748.ce.

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17

Wang, Hua, Wajahat Mehal, Laura E. Nagy, and Yaron Rotman. "Immunological mechanisms and therapeutic targets of fatty liver diseases." Cellular & Molecular Immunology 18, no. 1 (December 2, 2020): 73–91. http://dx.doi.org/10.1038/s41423-020-00579-3.

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AbstractAlcoholic liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD) are the two major types of chronic liver disease worldwide. Inflammatory processes play key roles in the pathogeneses of fatty liver diseases, and continuous inflammation promotes the progression of alcoholic steatohepatitis (ASH) and nonalcoholic steatohepatitis (NASH). Although both ALD and NAFLD are closely related to inflammation, their respective developmental mechanisms differ to some extent. Here, we review the roles of multiple immunological mechanisms and therapeutic targets related to the inflammation associated with fatty liver diseases and the differences in the progression of ASH and NASH. Multiple cell types in the liver, including macrophages, neutrophils, other immune cell types and hepatocytes, are involved in fatty liver disease inflammation. In addition, microRNAs (miRNAs), extracellular vesicles (EVs), and complement also contribute to the inflammatory process, as does intertissue crosstalk between the liver and the intestine, adipose tissue, and the nervous system. We point out that inflammation also plays important roles in promoting liver repair and controlling bacterial infections. Understanding the complex regulatory process of disrupted homeostasis during the development of fatty liver diseases may lead to the development of improved targeted therapeutic intervention strategies.
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18

Bonavita, André Gustavo, Kátia Quaresma, Vinícius Cotta-de-Almeida, Marcelo Alves Pinto, Roberto Magalhães Saraiva, and Luiz Anastácio Alves. "Hepatocyte xenotransplantation for treating liver disease." Xenotransplantation 17, no. 3 (June 9, 2010): 181–87. http://dx.doi.org/10.1111/j.1399-3089.2010.00588.x.

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19

Suzuki, Atsushi, Naho Sekiyama, Norihiko Koito, Yasuo Ohosone, Seiji Mita, Yasuo Matsuoka, and Shoichirou Irimajiri. "Liver disease in systemic lupus erythematosus." Japanese Journal of Clinical Immunology 18, no. 1 (1995): 53–59. http://dx.doi.org/10.2177/jsci.18.53.

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20

Mackay, Ian R., Janet M. Davies, and Merrill J. Rowley. "Towards the Pathogenesis of Autoimmune Liver Disease." Journal of Autoimmunity 13, no. 1 (August 1999): 163–69. http://dx.doi.org/10.1006/jaut.1999.0304.

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21

Adolph, Timon E., Christoph Grander, Alexander R. Moschen, and Herbert Tilg. "Liver–Microbiome Axis in Health and Disease." Trends in Immunology 39, no. 9 (September 2018): 712–23. http://dx.doi.org/10.1016/j.it.2018.05.002.

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22

Santiesteban-Lores, Lazara Elena, Milena Carvalho Carneiro, Lourdes Isaac, and Lorena Bavia. "Complement System in Alcohol-Associated Liver Disease." Immunology Letters 236 (August 2021): 37–50. http://dx.doi.org/10.1016/j.imlet.2021.05.007.

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23

Mathurin, Philippe, and Michael R. Lucey. "Alcohol, liver disease, and transplantation." Current Opinion in Organ Transplantation 23, no. 2 (April 2018): 175–79. http://dx.doi.org/10.1097/mot.0000000000000517.

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24

Beraza, Naiara, Yann Malato, Leif E. Sander, Malika Al-Masaoudi, Julia Freimuth, Dieter Riethmacher, Gregory J. Gores, Tania Roskams, Christian Liedtke, and Christian Trautwein. "Hepatocyte-specific NEMO deletion promotes NK/NKT cell– and TRAIL-dependent liver damage." Journal of Experimental Medicine 206, no. 8 (July 27, 2009): 1727–37. http://dx.doi.org/10.1084/jem.20082152.

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Nuclear factor κB (NF-κB) is one of the main transcription factors involved in regulating apoptosis, inflammation, chronic liver disease, and cancer progression. The IKK complex mediates NF-κB activation and deletion of its regulatory subunit NEMO in hepatocytes (NEMOΔhepa) triggers chronic inflammation and spontaneous hepatocellular carcinoma development. We show that NEMOΔhepa mice were resistant to Fas-mediated apoptosis but hypersensitive to tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) as the result of a strong up-regulation of its receptor DR5 on hepatocytes. Additionally, natural killer (NK) cells, the main source of TRAIL, were activated in NEMOΔhepa livers. Interestingly, depletion of the NK1.1+ cells promoted a significant reduction of liver inflammation and an improvement of liver histology in NEMOΔhepa mice. Furthermore, hepatocyte-specific NEMO deletion strongly sensitized the liver to concanavalin A (ConA)–mediated injury. The critical role of the NK cell/TRAIL axis in NEMOΔhepa livers during ConA hepatitis was further confirmed by selective NK cell depletion and adoptive transfer of TRAIL-deficient−/− mononuclear cells. Our results uncover an essential mechanism of NEMO-mediated protection of the liver by preventing NK cell tissue damage via TRAIL/DR5 signaling. As this mechanism is important in human liver diseases, NEMOΔhepa mice are an interesting tool to give insight into liver pathophysiology and to develop future therapeutic strategies.
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25

Selmi, Carlo, Maria De Santis, and M. Eric Gershwin. "Liver involvement in subjects with rheumatic disease." Arthritis Research & Therapy 13, no. 3 (2011): 226. http://dx.doi.org/10.1186/ar3319.

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26

Peters, Marion G. "Animal models of autoimmune liver disease." Immunology and Cell Biology 80, no. 1 (February 2002): 113–16. http://dx.doi.org/10.1046/j.0818-9641.2001.01059.x.

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27

Gooptu, Mahasweta, and John Koreth. "Translational and clinical advances in acute graft-versus-host disease." Haematologica 105, no. 11 (September 17, 2020): 2550–60. http://dx.doi.org/10.3324/haematol.2019.240309.

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Acute graft-versus-host disease (aGvHD) is induced by immunocompetent alloreactive T lymphocytes in the donor graft responding to polymorphic and non-polymorphic host antigens and causing inflammation in primarily the skin, gastrointestinal tract and liver. aGvHD remains an important toxicity of allogeneic transplantation, and the search for better prophylactic and therapeutic strategies is critical to improve transplant outcomes. In this review, we discuss the significant translational and clinical advances in the field which have evolved based on a better understanding of transplant immunology. Prophylactic advances have been primarily focused on the depletion of T lymphocytes and modulation of T-cell activation, proliferation, effector and regulatory functions. Therapeutic strategies beyond corticosteroids have focused on inhibiting key cytokine pathways, lymphocyte trafficking, and immunologic tolerance. We also briefly discuss important future trends in the field, the role of the intestinal microbiome and dysbiosis, as well as prognostic biomarkers for aGvHD which may improve stratification-based application of preventive and therapeutic strategies.
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28

Kasztelan-Szczerbinska, Beata, Agata Surdacka, Maria Slomka, Jacek Rolinski, Krzysztof Celinski, Halina Cichoz-Lach, Agnieszka Madro, and Mariusz Szczerbinski. "Angiogenesis-Related Biomarkers in Patients with Alcoholic Liver Disease: Their Association with Liver Disease Complications and Outcome." Mediators of Inflammation 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/673032.

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Angiogenesis is believed to be implicated in the pathogenesis of alcoholic liver disease (ALD). We aimed to explore the usefulness and accuracy of plasma angiogenic biomarkers for noninvasive evaluation of the severity of liver failure and ALD outcome. One hundred and forty-seven patients with ALD were prospectively enrolled and assessed based on their (1) gender, (2) age, (3) severity of liver dysfunction according to the Child-Turcotte-Pugh and MELD scores, and (4) the presence of ALD complications. Plasma levels of vascular endothelial growth factor (VEGF-A) and angiopoietins 1 and 2 (Ang1 and Ang2) were investigated using ELISAs. Multivariable logistic regression was applied in order to select independent predictors of advanced liver dysfunction and the disease complications. Significantly higher concentrations of Ang2 and VEGF-A in ALD patients as compared to controls were found. There was no difference in Ang1 levels in both groups. A positive correlation of Ang2 levels with INR (Rho 0.66;P<0.0001) and its inverse correlation with plasma albumin levels (Rho –0.62;P<0.0001) were found. High Ang2 concentrations turned out to be an independent predictor of severe liver dysfunction, as well as hepatic encephalopathy and renal impairment. Ang2 possessed the highest diagnostic and prognostic potential among three studied angiogenesis-related molecules.
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29

Loftus, Edward V., William J. Sandborn, Keith D. Lindor, and Nicholas F. LaRusso. "Interactions Between Chronic Liver Disease and Inflammatory Bowel Disease." Inflammatory Bowel Diseases 3, no. 4 (1997): 288–302. http://dx.doi.org/10.1097/00054725-199712000-00007.

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30

Loftus, Edward V., William J. Sandborn, Keith D. Lindor, and Nicholas F. Larusso. "Interactions between chronic liver disease and inflammatory bowel disease." Inflammatory Bowel Diseases 3, no. 4 (1997): 288–302. http://dx.doi.org/10.1002/ibd.3780030408.

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31

Liu, Kai, Fu-Sheng Wang, and Ruonan Xu. "Neutrophils in liver diseases: pathogenesis and therapeutic targets." Cellular & Molecular Immunology 18, no. 1 (November 6, 2020): 38–44. http://dx.doi.org/10.1038/s41423-020-00560-0.

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AbstractPreviously, it was assumed that peripheral neutrophils are a homogeneous population that displays antimicrobial functions. However, recent data have revealed that neutrophils are heterogeneous and are additionally involved in tissue damage and immune regulation. The phenotypic and functional plasticity of neutrophils has been identified in patients with cancer, inflammatory disorders, infections, and other diseases. Currently, neutrophils, with their autocrine, paracrine, and immune modulation functions, have been shown to be involved in liver diseases, including viral hepatitis, nonalcoholic steatohepatitis, alcoholic liver disease, liver fibrosis, cirrhosis, liver failure, and liver cancer. Accordingly, this review summarizes the role of neutrophils in liver diseases.
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32

Eksteen, Bertus, Allister J. Grant, Alice Miles, Stuart M. Curbishley, Patricia F. Lalor, Stefan G. Hübscher, Michael Briskin, Mike Salmon, and David H. Adams. "Hepatic Endothelial CCL25 Mediates the Recruitment of CCR9+ Gut-homing Lymphocytes to the Liver in Primary Sclerosing Cholangitis." Journal of Experimental Medicine 200, no. 11 (November 22, 2004): 1511–17. http://dx.doi.org/10.1084/jem.20041035.

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Primary sclerosing cholangitis (PSC), a chronic inflammatory liver disease characterized by progressive bile duct destruction, develops as an extra-intestinal complication of inflammatory bowel disease (IBD) (Chapman, R.W. 1991. Gut. 32:1433–1435). However, the liver and bowel inflammation are rarely concomitant, and PSC can develop in patients whose colons have been removed previously. We hypothesized that PSC is mediated by long-lived memory T cells originally activated in the gut, but able to mediate extra-intestinal inflammation in the absence of active IBD (Grant, A.J., P.F. Lalor, M. Salmi, S. Jalkanen, and D.H. Adams. 2002. Lancet. 359:150–157). In support of this, we show that liver-infiltrating lymphocytes in PSC include mucosal T cells recruited to the liver by aberrant expression of the gut-specific chemokine CCL25 that activates α4β7 binding to mucosal addressin cell adhesion molecule 1 on the hepatic endothelium. This is the first demonstration in humans that T cells activated in the gut can be recruited to an extra-intestinal site of disease and provides a paradigm to explain the pathogenesis of extra-intestinal complications of IBD.
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33

Bond, J. E., P. S. Kishnani, and D. D. Koeberl. "Immunomodulatory, liver depot gene therapy for Pompe disease." Cellular Immunology 342 (August 2019): 103737. http://dx.doi.org/10.1016/j.cellimm.2017.12.011.

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34

Pozzato, Gabriele, Michèle Moretti, Marina Crovatto, Maria Luisa Modolo, Daniele Gennari, and Gianfranco Santini. "Lymphocyte subsets in HCV-positive chronic liver disease." Immunology Today 15, no. 3 (March 1994): 137–38. http://dx.doi.org/10.1016/0167-5699(94)90159-7.

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35

Pelli, Fensom, Slade, Boa, Mieli-Vergani, and Vergani. "Argininosuccinate lyase: a new autoantigen in liver disease." Clinical & Experimental Immunology 114, no. 3 (December 1998): 455–61. http://dx.doi.org/10.1046/j.1365-2249.1998.00754.x.

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36

Henao-Mejia, Jorge, Eran Elinav, Christoph A. Thaiss, Paula Licona-Limon, and Richard A. Flavell. "Role of the intestinal microbiome in liver disease." Journal of Autoimmunity 46 (October 2013): 66–73. http://dx.doi.org/10.1016/j.jaut.2013.07.001.

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37

Santodomingo-Garzon, Tania, and Mark G. Swain. "Role of NKT cells in autoimmune liver disease." Autoimmunity Reviews 10, no. 12 (October 2011): 793–800. http://dx.doi.org/10.1016/j.autrev.2011.06.003.

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38

Albanis, E., and S. L. Friedman. "Antifibrotic Agents for Liver Disease." American Journal of Transplantation 6, no. 1 (January 2006): 12–19. http://dx.doi.org/10.1111/j.1600-6143.2005.01143.x.

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39

Fainboim, Leonardo, Alejandra Cherñavsky, Natalia Paladino, Ana C. Flores, and Lourdes Arruvito. "Cytokines and chronic liver disease." Cytokine & Growth Factor Reviews 18, no. 1-2 (February 2007): 143–57. http://dx.doi.org/10.1016/j.cytogfr.2007.01.017.

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40

Bardou, Franck-Nicolas, Olivier Guillaud, Domitille Erard-Poinsot, Christine Chambon-Augoyard, Elsa Thimonier, Mélanie Vallin, Olivier Boillot, and Jérôme Dumortier. "Tacrolimus exposure after liver transplantation for alcohol-related liver disease: Impact on complications." Transplant Immunology 56 (October 2019): 101227. http://dx.doi.org/10.1016/j.trim.2019.101227.

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41

Kamdar, Kala Y., Cliona M. Rooney, and Helen E. Heslop. "Posttransplant lymphoproliferative disease following liver transplantation." Current Opinion in Organ Transplantation 16, no. 3 (June 2011): 274–80. http://dx.doi.org/10.1097/mot.0b013e3283465715.

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42

Aledort, LM, PH Levine, M. Hilgartner, P. Blatt, JA Spero, JD Goldberg, L. Bianchi, V. Desmet, P. Scheuer, and H. Popper. "A study of liver biopsies and liver disease among hemophiliacs." Blood 66, no. 2 (August 1, 1985): 367–72. http://dx.doi.org/10.1182/blood.v66.2.367.367.

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Abstract Hepatic histologic materials (biopsy or autopsy) and associated clinical data from 155 hemophiliacs were collected by an ad hoc hemophilia study group and analyzed retrospectively in an effort to determine the spectrum of liver disease in this population and to examine the relationship between the severity of liver disease and treatment history. Clinical information on the frequency of complications from 126 biopsies in 115 hemophilic patients provided a unique opportunity to assess the safety of liver biopsy in such patients. The incidence of cirrhosis (15%) and chronic active hepatitis (7%) was lower than previously reported. The frequency of severe liver disease (chronic active hepatitis or cirrhosis) in patients receiving large pooled concentrates was no greater than in patients treated principally with cryoprecipitate or plasma. The risks of liver biopsy in this setting are relatively high: clinically significant hemorrhage followed 12.5% of the procedures.
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43

Aledort, LM, PH Levine, M. Hilgartner, P. Blatt, JA Spero, JD Goldberg, L. Bianchi, V. Desmet, P. Scheuer, and H. Popper. "A study of liver biopsies and liver disease among hemophiliacs." Blood 66, no. 2 (August 1, 1985): 367–72. http://dx.doi.org/10.1182/blood.v66.2.367.bloodjournal662367.

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Hepatic histologic materials (biopsy or autopsy) and associated clinical data from 155 hemophiliacs were collected by an ad hoc hemophilia study group and analyzed retrospectively in an effort to determine the spectrum of liver disease in this population and to examine the relationship between the severity of liver disease and treatment history. Clinical information on the frequency of complications from 126 biopsies in 115 hemophilic patients provided a unique opportunity to assess the safety of liver biopsy in such patients. The incidence of cirrhosis (15%) and chronic active hepatitis (7%) was lower than previously reported. The frequency of severe liver disease (chronic active hepatitis or cirrhosis) in patients receiving large pooled concentrates was no greater than in patients treated principally with cryoprecipitate or plasma. The risks of liver biopsy in this setting are relatively high: clinically significant hemorrhage followed 12.5% of the procedures.
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44

Allen, K. J., N. E. Buck, and R. Williamson. "Stem cells for the treatment of liver disease." Transplant Immunology 15, no. 2 (December 2005): 99–112. http://dx.doi.org/10.1016/j.trim.2005.09.001.

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45

Schiavon, Leonardo L., Roberto J. Carvalho-Filho, Janaína Luz Narciso-Schiavon, Valéria P. Lanzoni, Maria Lucia G. Ferraz, and Antonio Eduardo B. Silva. "Late-onset systemic lupus erythematosus-associated liver disease." Rheumatology International 32, no. 9 (April 8, 2010): 2917–20. http://dx.doi.org/10.1007/s00296-010-1492-4.

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46

Yang, Cheng, Xiaoqing He, Jinqiu Zhao, and Wenxiang Huang. "Hepatoprotection by Ginsenoside Rg1 in alcoholic liver disease." International Immunopharmacology 92 (March 2021): 107327. http://dx.doi.org/10.1016/j.intimp.2020.107327.

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47

Menon, Jagadeesh, Naresh Shanmugam, Anu Vasudevan, Narendra Kumar, Ashwin Rammohan, and Mohamed Rela. "Kawasaki disease in a pediatric liver transplant patient." Transplant Immunology 67 (August 2021): 101416. http://dx.doi.org/10.1016/j.trim.2021.101416.

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48

Galle, P. R., W. J. Hofmann, H. Walczak, H. Schaller, G. Otto, W. Stremmel, P. H. Krammer, and L. Runkel. "Involvement of the CD95 (APO-1/Fas) receptor and ligand in liver damage." Journal of Experimental Medicine 182, no. 5 (November 1, 1995): 1223–30. http://dx.doi.org/10.1084/jem.182.5.1223.

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Apoptosis occurs in the normal liver and in various forms of liver disease. The CD95 (APO-1/Fas) (CD95) receptor mediates apoptosis, and liver cells in animal models are acutely sensitive to apoptosis initiated by this receptor. We have used primary human hepatocytes as a model system to investigate CD95-mediated apoptotic liver damage. Treatment of fresh human hepatocytes with low concentrations of agonistic antibodies against CD95 resulted in apoptosis of &gt; 95% of the cultured liver cells within 4 and 7.5 h. Immunohistology of a panel of explanted liver tissues revealed that hepatocytes in normal livers (n = 5) and in alcoholic cirrhosis (n = 13) expressed low constitutive levels of CD95. CD95 receptor expression was highly elevated in hepatocytes in hepatitis B virus-related cirrhosis (n = 9) and in acute liver failure (n = 8). By in situ hybridization CD95 ligand messenger RNA expression was absent in normal liver but detected at high levels in livers with ongoing liver damage. In cases of hepatitis B virus-related cirrhosis and acute hepatic failure, ligand expression was found primarily in areas with lymphocytic infiltration. In contrast, in patients with alcoholic liver damage, high CD95 ligand messenger RNA expression was found in hepatocytes. These findings suggest that liver destruction in hepatitis B may primarily involve killing of hepatocytes by T lymphocytes using the CD95 receptor-ligand system. In alcoholic liver damage, death of hepatocytes might occur by fratricide and paracrine or autocrine mechanisms mediated by the hepatocytes themselves.
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49

Neff, Guy W., Dushyantha Jayaweera, and Andreas G. Tzakis. "Liver transplantation for HIV-infected patients with end-stage liver disease." Current Opinion in Organ Transplantation 7, no. 2 (June 2002): 114–23. http://dx.doi.org/10.1097/00075200-200206000-00002.

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50

Macpherson, Iain, Jennifer H. Nobes, Eleanor Dow, Elizabeth Furrie, Michael H. Miller, Emma M. Robinson, and John F. Dillon. "Intelligent Liver Function Testing: Working Smarter to Improve Patient Outcomes in Liver Disease." Journal of Applied Laboratory Medicine 5, no. 5 (September 1, 2020): 1090–100. http://dx.doi.org/10.1093/jalm/jfaa109.

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Abstract Chronic liver disease (CLD) is a significant health problem affecting millions of people worldwide. In Scotland, CLD is a major cause of premature mortality. Liver function tests (LFTs) are a panel of frequently requested blood tests which may indicate liver disease. However, LFTs commonly contain at least one abnormal result, and abnormalities are rarely investigated to the extent recommended by national guidelines. The intelligent Liver Function Testing (iLFT) pathway is a novel, automated system designed to improve early diagnosis of liver disease. Initial abnormal LFT results trigger a cascade of reflexive testing to help identify the cause of any liver dysfunction. Algorithms combine these results with demographic and clinical data (such as patient age, body mass index, and alcohol intake) and fibrosis estimates to produce an electronic diagnosis and management plan. The pilot trial demonstrated that iLFT increased diagnosis of liver disease whilst remaining cost-effective. As such, iLFT has been fully operational across our region (NHS Tayside, Scotland) since August 2018. In the first year, iLFT generated over 2000 diagnoses from 1824 patient samples with an abnormality in the initial LFTs. The majority of these patients could be safely managed in primary care. iLFT allows maximal value to be obtained from liver blood tests across biochemistry, virology, immunology, and hematology with only minor changes to working practices. ‘Intelligent’, algorithm-led testing pathways break down the barrier between clinical and laboratory medicine and offer solutions to many of the challenges experienced in modern healthcare systems.
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