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The bidirectional immune crosstalk in metabolic dysfunction-associated steatotic liver disease
Open accessAbstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) is an unabated risk factor for end-stage liver diseases with no available therapies. Dysregulated immune responses are critical culprits of MASLD pathogenesis. Independent contributions from either the innate or adaptive arms of the immune system or their unidirectional interplay are commonly studied in MASLD. However, the bidirectional communication between innate and adaptive immune systems and its impact on MASLD remain insufficiently understood. Given that both innate and adaptive immune cells are indispensable for the development and progression of inflammation in MASLD, elucidating pathogenic contributions stemming from the bidirectional interplay between these two arms holds potential for development of novel therapeutics for MASLD. Here, we review the immune cell types and bidirectional pathways that influence the pathogenesis of MASLD and highlight potential pharmacologic approaches to combat MASLD based on current knowledge of this bidirectional crosstalk.
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“The roles of Tregs in MASLD and MASH remain unclear, with emerging evidence suggesting that their hepatic accumulation and functional relevance may vary depending on the disease model employed (Sawada et al. 2023).”
From The double-edged sword of regulatory T cells in MASLD: from inflammation control to fibrosis promotion (2026) · cites this paper as Sawada et al. 2023
Citations
Cites
A multisociety Delphi consensus statement on new fatty liver disease nomenclature
Rinella, M. E., Lazarus, J. V., Ratziu, V., Francque, S. M., Sanyal, A. J., Kanwal, F., Romero, D., Abdelmalek, M. F., Anstee, Q. M., Arab, J. P., et al. (2023) · Hepatology · doi:10.1097/hep.0000000000000520 · Cited by 3,476
Type I interferons in infectious disease
McNab, F., Mayer-Barber, K., Sher, A., Wack, A., & O'Garra, A. (2015) · Nature Reviews Immunology · doi:10.1038/nri3787 · Cited by 2,780
Rinella, M. E., Neuschwander-Tetri, B. A., Siddiqui, M. S., Abdelmalek, M. F., Caldwell, S., Barb, D., Kleiner, D. E., & Loomba, R. (2023) · Hepatology · doi:10.1097/hep.0000000000000323 · Cited by 2,667
Inflammasome-mediated dysbiosis regulates progression of NAFLD and obesity
Henao-Mejia, J., Elinav, E., Jin, C., Hao, L., Mehal, W. Z., Strowig, T., Thaiss, C. A., Kau, A. L., Eisenbarth, S. C., Jurczak, M. J., et al. (2012) · Nature · doi:10.1038/nature10809 · Cited by 2,435
Type 2 immunity in tissue repair and fibrosis
Gieseck, R. L., Wilson, M. S., & Wynn, T. A. (2018) · Nature Reviews Immunology · doi:10.1038/nri.2017.90 · Cited by 1,055
Western Diet and the Immune System: An Inflammatory Connection
Christ, A., Lauterbach, M., & Latz, E. (2019) · Immunity · doi:10.1016/j.immuni.2019.09.020 · Cited by 907
The complex link between NAFLD and type 2 diabetes mellitus - mechanisms and treatments
Targher, G., Corey, K. E., Byrne, C. D., & Roden, M. (2021) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-021-00448-y · Cited by 850
A multisociety Delphi consensus statement on new fatty liver disease nomenclature
Rinella, M. E., Lazarus, J. V., Ratziu, V., Francque, S. M., Sanyal, A. J., Kanwal, F., Romero, D., Abdelmalek, M. F., Anstee, Q. M., Arab, J. P., et al. (2024) · Annals of Hepatology · doi:10.1016/j.aohep.2023.101133 · Cited by 844
CD28-mediated co-stimulation: a quantitative support for TCR signalling.
Acuto, O., & Michel, F. (2003) · Nature Reviews Immunology · doi:10.1038/nri1248 · Cited by 775
NAFLD causes selective CD4+ T lymphocyte loss and promotes hepatocarcinogenesis
Ma, C., Kesarwala, A. H., Eggert, T., Medina-Echeverz, J., Kleiner, D. E., Jin, P., Stroncek, D. F., Terabe, M., Kapoor, V., ElGindi, M., et al. (2016) · Nature · doi:10.1038/nature16969 · Cited by 766
Wolf, M. J., Adili, A., Piotrowitz, K., Abdullah, Z., Boege, Y., Stemmer, K., Ringelhan, M., Simonavicius, N., Egger, M., Wohlleber, D., et al. (2014) · Cancer Cell · doi:10.1016/j.ccell.2014.09.003 · Cited by 678
Auto-aggressive CXCR6+ CD8 T cells cause liver immune pathology in NASH
Dudek, M., Pfister, D., Donakonda, S., Filpe, P., Schneider, A., Laschinger, M., Hartmann, D., Hüser, N., Meiser, P., Bayerl, F., et al. (2021) · Nature · doi:10.1038/s41586-021-03233-8 · Cited by 518
Hepatic recruitment of macrophages promotes nonalcoholic steatohepatitis through CCR2
Miura, K., Yang, L., van Rooijen, N., Ohnishi, H., & Seki, E. (2012) · American Journal of Physiology-Gastrointestinal and Liver Physiology · doi:10.1152/ajpgi.00365.2011 · Cited by 503
Saravia, J., Chapman, N. M., & Chi, H. (2019) · Cellular & Molecular Immunology · doi:10.1038/s41423-019-0220-6 · Cited by 489
Tran, S., Baba, I., Poupel, L., Dussaud, S., Moreau, M., Gélineau, A., Marcelin, G., Magréau-Davy, E., Ouhachi, M., Lesnik, P., et al. (2020) · Immunity · doi:10.1016/j.immuni.2020.06.003 · Cited by 400
Can we use old NAFLD data under the new MASLD definition?
Song, S. J., Lai, J. C.-T., Wong, G. L.-H., Wong, V. W.-S., & Yip, T. C.-F. (2024) · Journal of Hepatology · doi:10.1016/j.jhep.2023.07.021 · Cited by 374
Adaptive immunity: an emerging player in the progression of NAFLD
Sutti, S., & Albano, E. (2020) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-019-0210-2 · Cited by 374
Rau, M., Schilling, A.-K., Meertens, J., Hering, I., Weiss, J., Jurowich, C., Kudlich, T., Hermanns, H. M., Bantel, H., Beyersdorf, N., et al. (2016) · The Journal of Immunology · doi:10.4049/jimmunol.1501175 · Cited by 302
Adaptive immune responses triggered by oxidative stress contribute to hepatic inflammation in NASH
Sutti, S., Jindal, A., Locatelli, I., Vacchiano, M., Gigliotti, L., Bozzola, C., & Albano, E. (2014) · Hepatology · doi:10.1002/hep.26749 · Cited by 270
Alkhouri, N., Morris‐Stiff, G., Campbell, C., Lopez, R., Tamimi, T. A., Yerian, L., Zein, N. N., & Feldstein, A. E. (2012) · Liver International · doi:10.1111/j.1478-3231.2011.02639.x · Cited by 256
Bertola, A., Bonnafous, S., Anty, R., Patouraux, S., Saint-Paul, M.-C., Iannelli, A., Gugenheim, J., Barr, J., Mato, J. M., Le Marchand-Brustel, Y., et al. (2010) · PLoS ONE · doi:10.1371/journal.pone.0013577 · Cited by 240
The Differential Roles of T Cells in Non-alcoholic Fatty Liver Disease and Obesity
Van Herck, M. A., Weyler, J., Kwanten, W. J., Dirinck, E. L., De Winter, B. Y., Francque, S. M., & Vonghia, L. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.00082 · Cited by 238
The Role of Innate Immune Cells in Nonalcoholic Steatohepatitis
Cai, J., Zhang, X., & Li, H. (2019) · Hepatology · doi:10.1002/hep.30506 · Cited by 207
Type I Interferon Responses Drive Intrahepatic T Cells to Promote Metabolic Syndrome
Ghazarian, M., Revelo, X. S., Nøhr, M. K., Luck, H., Zeng, K., Lei, H., Tsai, S., Schroer, S. A., Park, Y. J., Chng, M. H. Y., et al. (2017) · Science Immunology · doi:10.1126/sciimmunol.aai7616 · Cited by 190
Dendritic Cells Limit Fibroinflammatory Injury in Nonalcoholic Steatohepatitis in Mice
Henning, J. R., Graffeo, C. S., Rehman, A., Fallon, N. C., Zambirinis, C. P., Ochi, A., Barilla, R., Jamal, M., Deutsch, M., Greco, S., et al. (2013) · Hepatology · doi:10.1002/hep.26267 · Cited by 185
Characterization of Distinct Subpopulations of Hepatic Macrophages in HFD/Obese Mice
Morinaga, H., Mayoral, R., Heinrichsdorff, J., Osborn, O., Franck, N., Hah, N., Walenta, E., Bandyopadhyay, G., Pessentheiner, A. R., Chi, T. J., et al. (2015) · Diabetes · doi:10.2337/db14-1238 · Cited by 175
Self-citationRolla, S., Alchera, E., Imarisio, C., Bardina, V., Valente, G., Cappello, P., Mombello, C., Follenzi, A., Novelli, F., & Carini, R. (2016) · Clinical Science · doi:10.1042/cs20150405 · Cited by 158
Bruzzì, S., Sutti, S., Giudici, G., Burlone, M. E., Ramavath, N. N., Toscani, A., Bozzola, C., Schneider, P., Morello, E., Parola, M., et al. (2018) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2018.06.015 · Cited by 139
Giles, D. A., Moreno-Fernandez, M. E., Stankiewicz, T. E., Cappelletti, M., Huppert, S. S., Iwakura, Y., Dong, C., Shanmukhappa, S. K., & Divanovic, S. (2016) · PLOS ONE · doi:10.1371/journal.pone.0149783 · Cited by 116
Self-citationRevisiting the Role of Natural Killer Cells in Non-Alcoholic Fatty Liver Disease
Martínez-Chantar, M. L., Delgado, T. C., & Beraza, N. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.640869 · Cited by 67
Biologic and checkpoint inhibitor‐induced liver injury: a systematic literature review
Shah, P., Sundaram, V., & Björnsson, E. (2020) · Hepatology Communications · doi:10.1002/hep4.1465 · Cited by 64
The Detrimental Role of Regulatory T Cells in Nonalcoholic Steatohepatitis
Dywicki, J., Buitrago‐Molina, L. E., Noyan, F., Davalos‐Misslitz, A. C., Hupa‐Breier, K. L., Lieber, M., Hapke, M., Schlue, J., Falk, C. S., Raha, S., et al. (2022) · Hepatology Communications · doi:10.1002/hep4.1807 · Cited by 57
Group 3 innate lymphoid cells protect steatohepatitis from high-fat diet induced toxicity
Hamaguchi, M., Okamura, T., Fukuda, T., Nishida, K., Yoshimura, Y., Hashimoto, Y., Ushigome, E., Nakanishi, N., Majima, S., Asano, M., et al. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.648754 · Cited by 47
Dual roles of B lymphocytes in mouse models of diet-induced nonalcoholic fatty liver disease
Karl, M., Hasselwander, S., Zhou, Y., Reifenberg, G., Kim, Y. O., Park, K., Ridder, D. A., Wang, X., Seidel, E., Hövelmeyer, N., et al. (2022) · Hepatology · doi:10.1002/hep.32428 · Cited by 44
Nakamura, Y., Abe, M., Kawasaki, K., Miyake, T., Watanabe, T., Yoshida, O., Hirooka, M., Matsuura, B., & Hiasa, Y. (2019) · Scientific Reports · doi:10.1038/s41598-018-37403-y · Cited by 34
Research works printed but not linked: 279
- Sarwar, 2018, Obesity and nonalcoholic fatty liver disease: current perspectives, Diabetes Metab. Syndr. Obes., 11, 533, 10.2147/DMSO.S146339 · DOI
- Rinella, 2015, Nonalcoholic fatty liver disease: a systematic review, JAMA, 313, 2263, 10.1001/jama.2015.5370 · DOI
- Singh, 2015, Fibrosis progression in nonalcoholic fatty liver vs nonalcoholic steatohepatitis: a systematic review and meta-analysis of paired-biopsy studies, Clin. Gastroenterol. Hepatol., 13, 643, 10.1016/j.cgh.2014.04.014 · DOI · Paper page
- Zhai, 2021, The incidence trends of liver cirrhosis caused by nonalcoholic steatohepatitis via the GBD study 2017, Sci. Rep., 11, 5195, 10.1038/s41598-021-84577-z · DOI
- Younes, 2018, Should we undertake surveillance for HCC in patients with NAFLD?, J. Hepatol., 68, 326, 10.1016/j.jhep.2017.10.006 · DOI
- Goyal, 2016, The progression and natural history of pediatric nonalcoholic fatty liver disease, Clin. Liver Dis., 20, 325, 10.1016/j.cld.2015.10.003 · DOI
- Mitsinikos, 2021, Pediatric nonalcoholic fatty liver disease, Pediatr. Clin. North Am., 68, 1309, 10.1016/j.pcl.2021.07.013 · DOI
- Jobira, 2021, Hepatic steatosis relates to gastrointestinal microbiota changes in obese girls with polycystic ovary syndrome, PLoS One, 16, 10.1371/journal.pone.0245219 · DOI
- Wang, 2022, Paediatric non-alcoholic fatty liver disease: an approach to pathological evaluation, J. Clin. Pathol., 75, 443, 10.1136/jclinpath-2022-208246 · DOI
- Vos, 2022, Randomized placebo-controlled trial of losartan for pediatric NAFLD, Hepatology, 76, 429, 10.1002/hep.32403 · DOI
- Younossi, 2019, Nonalcoholic steatohepatitis is the fastest growing cause of hepatocellular carcinoma in liver transplant candidates, Clin. Gastroenterol. Hepatol., 17, 748, 10.1016/j.cgh.2018.05.057 · DOI
- Noureddin, 2018, NASH leading cause of liver transplant in women: updated analysis of indications for liver transplant and ethnic and gender variances, Am. J. Gastroenterol., 113, 1649, 10.1038/s41395-018-0088-6 · DOI
- Adam, 2018, 2018 Annual Report of the European Liver Transplant Registry (ELTR) - 50-year evolution of liver transplantation, Transpl. Int., 31, 1293, 10.1111/tri.13358 · DOI · Paper page
- Nababan, 2022, Portal hypertension in nonalcoholic fatty liver disease: from pathogenesis to clinical practice, J. Clin. Transl. Hepatol., 10, 979, 10.14218/JCTH.2021.00593 · DOI
- Anstee, 2013, Progression of NAFLD to diabetes mellitus, cardiovascular disease or cirrhosis, Nat. Rev. Gastroenterol. Hepatol., 10, 330, 10.1038/nrgastro.2013.41 · DOI · Paper page
- Ferguson, 2021, Emerging therapeutic approaches for the treatment of NAFLD and type 2 diabetes mellitus, Nat. Rev. Endocrinol., 17, 484, 10.1038/s41574-021-00507-z · DOI
- De Masi, 2023, Cyclo(His-Pro): a further step in the management of steatohepatitis, JHEP Rep., 5
- Sakaguchi, 2011, Progression of alcoholic and non-alcoholic steatohepatitis: common metabolic aspects of innate immune system and oxidative stress, Drug Metab. Pharmacokinet., 26, 30, 10.2133/dmpk.DMPK-10-RV-087 · DOI
- Farrell, 2012, NASH is an inflammatory disorder: pathogenic, prognostic and therapeutic implications, Gut Liver, 6, 149, 10.5009/gnl.2012.6.2.149 · DOI
- Alkhouri, 2009, Lipotoxicity in nonalcoholic fatty liver disease: not all lipids are created equal, Expert Rev. Gastroenterol. Hepatol., 3, 445, 10.1586/egh.09.32 · DOI
- Delli Bovi, 2021, Oxidative stress in non-alcoholic fatty liver disease. An updated mini review, Front. Med., 8, 10.3389/fmed.2021.595371 · DOI
- Ma, 2021, Oxidative stress is a key modulator in the development of nonalcoholic fatty liver disease, Antioxidants, 11, 91, 10.3390/antiox11010091 · DOI
- He, 2021, Gut microbiome-mediated alteration of immunity, inflammation, and metabolism involved in the regulation of non-alcoholic fatty liver disease, Front. Microbiol., 12, 10.3389/fmicb.2021.761836 · DOI
- Reccia, 2017, Non-alcoholic fatty liver disease: a sign of systemic disease, Metabolism, 72, 94, 10.1016/j.metabol.2017.04.011 · DOI
- Fotbolcu, 2016, Nonalcoholic fatty liver disease as a multi-systemic disease, World J. Gastroenterol., 22, 4079, 10.3748/wjg.v22.i16.4079 · DOI
- Marques, 2023, Overview of cellular and soluble mediators in systemic inflammation associated with non-alcoholic fatty liver disease, Int. J. Mol. Sci., 24, 2313, 10.3390/ijms24032313 · DOI
- Wang, 2021, Recent advances in adipose tissue dysfunction and its role in the pathogenesis of non-alcoholic fatty liver disease, Cells, 10, 3300, 10.3390/cells10123300 · DOI
- Cordeiro, 2020, Does adipose tissue inflammation drive the development of non-alcoholic fatty liver disease in obesity?, Clin. Res. Hepatol. Gastroenterol., 44, 394, 10.1016/j.clinre.2019.10.001 · DOI
- Altajar, 2020, Skeletal muscle dysfunction in the development and progression of nonalcoholic fatty liver disease, J. Clin. Transl. Hepatol., 8, 414
- Bhanji, 2017, Sarcopenia in hiding: the risk and consequence of underestimating muscle dysfunction in nonalcoholic steatohepatitis, Hepatology, 66, 2055, 10.1002/hep.29420 · DOI
- Giles, 2017, Thermoneutral housing exacerbates nonalcoholic fatty liver disease in mice and allows for sex-independent disease modeling, Nat. Med., 23, 829, 10.1038/nm.4346 · DOI
- Machado, 2015, Mouse models of diet-induced nonalcoholic steatohepatitis reproduce the heterogeneity of the human disease, PLoS One, 10
- Rinella, 2008, Mechanisms of hepatic steatosis in mice fed a lipogenic methionine choline-deficient diet, J. Lipid Res., 49, 1068, 10.1194/jlr.M800042-JLR200 · DOI
- Denda, 2002, Development of hepatocellular adenomas and carcinomas associated with fibrosis in C57BL/6J male mice given a choline-deficient, L-amino acid-defined diet, Jpn. J. Cancer Res., 93, 125, 10.1111/j.1349-7006.2002.tb01250.x · DOI
- Boll, 2001, Mechanism of carbon tetrachloride-induced hepatotoxicity. Hepatocellular damage by reactive carbon tetrachloride metabolites, Z. Naturforsch., C: J. Biosci., 56, 649, 10.1515/znc-2001-7-826 · DOI
- Ito, 2007, Longitudinal analysis of murine steatohepatitis model induced by chronic exposure to high-fat diet, Hepatol. Res., 37, 50, 10.1111/j.1872-034X.2007.00008.x · DOI
- Oates, 2023, Thermoneutral housing shapes hepatic inflammation and damage in mouse models of non-alcoholic fatty liver disease, Front. Immunol., 14, 10.3389/fimmu.2023.1095132 · DOI
- Davidson, 2001, Autoimmune diseases, N. Engl. J. Med., 345, 340, 10.1056/NEJM200108023450506 · DOI
- O'Shea, 2002, Cytokines and autoimmunity, Nat. Rev. Immunol., 2, 37, 10.1038/nri702 · DOI
- Carter-Kent, 2008, Cytokines in the pathogenesis of fatty liver and disease progression to steatohepatitis: implications for treatment, Am. J. Gastroenterol., 103, 1036, 10.1111/j.1572-0241.2007.01709.x · DOI
- Gasteiger, 2014, Interactions between innate and adaptive lymphocytes, Nat. Rev. Immunol., 14, 631, 10.1038/nri3726 · DOI
- Strutt, 2011, Control of innate immunity by memory CD4 T cells, Adv. Exp. Med. Biol., 780, 57, 10.1007/978-1-4419-5632-3_6 · DOI
- Swain, 2012, Expanding roles for CD4(+) T cells in immunity to viruses, Nat. Rev. Immunol., 12, 136, 10.1038/nri3152 · DOI
- Soudja, 2014, Memory-T-cell-derived interferon-gamma instructs potent innate cell activation for protective immunity, Immunity, 40, 974, 10.1016/j.immuni.2014.05.005 · DOI
- Jain, 2020, T cells instruct myeloid cells to produce inflammasome-independent IL-1beta and cause autoimmunity, Nat. Immunol., 21, 65, 10.1038/s41590-019-0559-y · DOI
- McDaniel, 2022, Effector memory CD4(+) T cells induce damaging innate inflammation and autoimmune pathology by engaging CD40 and TNFR on myeloid cells, Sci. Immunol., 7
- Huby, 2022, Immune cell-mediated features of non-alcoholic steatohepatitis, Nat. Rev. Immunol., 22, 429, 10.1038/s41577-021-00639-3 · DOI · Paper page
- Zhan, 2010, Roles of liver innate immune cells in nonalcoholic fatty liver disease, World J. Gastroenterol., 16, 4652, 10.3748/wjg.v16.i37.4652 · DOI
- Maher, 2008, Beyond insulin resistance: innate immunity in nonalcoholic steatohepatitis, Hepatology, 48, 670, 10.1002/hep.22399 · DOI
- Park, 2023, Major roles of Kupffer cells and macrophages in NAFLD development, Front. Endocrinol., 14, 10.3389/fendo.2023.1150118 · DOI
- Xu, 2023, Activation of Kupffer cells in NAFLD and NASH: mechanisms and therapeutic interventions, Front. Cell Dev. Biol., 11, 10.3389/fcell.2023.1199519 · DOI
- Barreby, 2022, Macrophage functional diversity in NAFLD - more than inflammation, Nat. Rev. Endocrinol., 18, 461, 10.1038/s41574-022-00675-6 · DOI
- Rivera, 2007, Toll-like receptor-4 signaling and Kupffer cells play pivotal roles in the pathogenesis of non-alcoholic steatohepatitis, J. Hepatol., 47, 571, 10.1016/j.jhep.2007.04.019 · DOI · Paper page
- Ye, 2012, Toll-like receptor-4 mediates obesity-induced non-alcoholic steatohepatitis through activation of X-box binding protein-1 in mice, Gut, 61, 1058, 10.1136/gutjnl-2011-300269 · DOI · Paper page
- Kremer, 2010, Kupffer cell and interleukin-12-dependent loss of natural killer T cells in hepatosteatosis, Hepatology, 51, 130, 10.1002/hep.23292 · DOI
- Bieghs, 2013, The innate immune response during liver inflammation and metabolic disease, Trends Immunol., 34, 446, 10.1016/j.it.2013.04.005 · DOI
- Oates, 2019, Macrophage function in the pathogenesis of non-alcoholic fatty liver disease: the mac attack, Front. Immunol., 10, 2893, 10.3389/fimmu.2019.02893 · DOI
- Reid, 2016, Kupffer cells undergo fundamental changes during the development of experimental NASH and are critical in initiating liver damage and inflammation, PLoS One, 11, 10.1371/journal.pone.0159524 · DOI
- Seidman, 2020, Niche-specific reprogramming of epigenetic landscapes drives myeloid cell diversity in nonalcoholic steatohepatitis, Immunity, 52, 1057, 10.1016/j.immuni.2020.04.001 · DOI · Paper page
- Remmerie, 2020, Osteopontin expression identifies a subset of recruited macrophages distinct from Kupffer cells in the fatty liver, Immunity, 53, 641, 10.1016/j.immuni.2020.08.004 · DOI · Paper page
- Kazankov, 2019, The role of macrophages in nonalcoholic fatty liver disease and nonalcoholic steatohepatitis, Nat. Rev. Gastroenterol. Hepatol., 16, 145, 10.1038/s41575-018-0082-x · DOI · Paper page
- McDonald, 2013, Kupffer cells and activation of endothelial TLR4 coordinate neutrophil adhesion within liver sinusoids during endotoxemia, Am. J. Physiol. Gastrointest. Liver Physiol., 305, G797, 10.1152/ajpgi.00058.2013 · DOI
- Cho, 2021, Two faces of neutrophils in liver disease development and progression, Hepatology, 74, 503, 10.1002/hep.31680 · DOI
- Paquissi, 2016, Immune imbalances in non-alcoholic fatty liver disease: from general biomarkers and neutrophils to interleukin-17 axis activation and new therapeutic targets, Front. Immunol., 7, 490, 10.3389/fimmu.2016.00490 · DOI
- Giles, 2015, IL-17 axis driven inflammation in non-alcoholic fatty liver disease progression, Curr. Drug Targets, 16, 1315, 10.2174/1389450116666150531153627 · DOI
- Pulli, 2015, Myeloperoxidase-hepatocyte-stellate cell cross talk promotes hepatocyte injury and fibrosis in experimental nonalcoholic steatohepatitis, Antioxid. Redox Signal., 23, 1255, 10.1089/ars.2014.6108 · DOI · Paper page
- Gadd, 2014, The portal inflammatory infiltrate and ductular reaction in human nonalcoholic fatty liver disease, Hepatology, 59, 1393, 10.1002/hep.26937 · DOI · Paper page
- Zhao, 2020, Neutrophils undergo switch of apoptosis to NETosis during murine fatty liver injury via S1P receptor 2 signaling, Cell Death Dis., 11, 379, 10.1038/s41419-020-2582-1 · DOI
- van der Windt, 2018, Neutrophil extracellular traps promote inflammation and development of hepatocellular carcinoma in nonalcoholic steatohepatitis, Hepatology, 68, 1347, 10.1002/hep.29914 · DOI
- Thomas, 2023, Neutrophil-lymphocyte ratio in relation to risk of hepatocellular carcinoma in patients with non-alcoholic fatty liver disease, Cancer Med., 12, 3589, 10.1002/cam4.5185 · DOI
- Bernsmeier, 2017, Liver dendritic cells and NAFLD evolution: a remaining open issue, J. Hepatol., 66, 1120, 10.1016/j.jhep.2017.02.018 · DOI
- Sutti, 2015, CX3CR1-expressing inflammatory dendritic cells contribute to the progression of steatohepatitis, Clin. Sci., 129, 797, 10.1042/CS20150053 · DOI
- Thomson, 2010, Antigen-presenting cell function in the tolerogenic liver environment, Nat. Rev. Immunol., 10, 753, 10.1038/nri2858 · DOI
- Heymann, 2016, Immunology in the liver--from homeostasis to disease, Nat. Rev. Gastroenterol. Hepatol., 13, 88, 10.1038/nrgastro.2015.200 · DOI · Paper page
- van der Zande, 2023, Dendritic cell-intrinsic LKB1-AMPK/SIK signaling controls metabolic homeostasis by limiting the hepatic Th17 response during obesity, JCI Insight, 8, 10.1172/jci.insight.157948 · DOI
- Bernsmeier, 2017, Liver dendritic cells and NAFLD evolution: a remaining open issue, J. Hepatol., 66, 1120, 10.1016/j.jhep.2017.02.018 · DOI
- Peng, 2017, Diversity of tissue-resident NK cells, Semin. Immunol., 31, 3, 10.1016/j.smim.2017.07.006 · DOI
- Tian, 2013, Natural killer cells in liver disease, Hepatology, 57, 1654, 10.1002/hep.26115 · DOI
- Luci, 2019, Natural killer cells and type 1 innate lymphoid cells are new actors in non-alcoholic fatty liver disease, Front. Immunol., 10, 1192, 10.3389/fimmu.2019.01192 · DOI
- Diedrich, 2020, Characterization of the immune cell landscape of patients with NAFLD, PLoS One, 15, 10.1371/journal.pone.0230307 · DOI
- Kahraman, 2010, Major histocompatibility complex class I-related chains A and B (MIC A/B): a novel role in nonalcoholic steatohepatitis, Hepatology, 51, 92, 10.1002/hep.23253 · DOI
- Cuff, 2019, The obese liver environment mediates conversion of NK cells to a less cytotoxic ILC1-like phenotype, Front. Immunol., 10, 2180, 10.3389/fimmu.2019.02180 · DOI
- Hoechst, 2009, Myeloid derived suppressor cells inhibit natural killer cells in patients with hepatocellular carcinoma via the NKp30 receptor, Hepatology, 50, 799, 10.1002/hep.23054 · DOI
- Koo, 2020, Immunological distinctions between nonalcoholic steatohepatitis and hepatocellular carcinoma, Exp. Mol. Med., 52, 1209, 10.1038/s12276-020-0480-3 · DOI · Paper page
- Cui, 2019, NKT cells in neurological diseases, Front. Cell. Neurosci., 13, 245, 10.3389/fncel.2019.00245 · DOI
- Martin-Murphy, 2014, Mice lacking natural killer T cells are more susceptible to metabolic alterations following high fat diet feeding, PLoS One, 9, 10.1371/journal.pone.0080949 · DOI
- Miyagi, 2010, Absence of invariant natural killer T cells deteriorates liver inflammation and fibrosis in mice fed high-fat diet, J. Gastroenterol., 45, 1247, 10.1007/s00535-010-0272-y · DOI
- Han, 2023, Invariant natural killer T cells drive hepatic homeostasis in nonalcoholic fatty liver disease via sustained IL-10 expression in CD170(+) Kupffer cells, Eur. J. Immunol., 10.1002/eji.202350474 · DOI
- Liew, 2017, iNKT cells orchestrate a switch from inflammation to resolution of sterile liver injury, Immunity, 47, 752, 10.1016/j.immuni.2017.09.016 · DOI · Paper page
- Anson, 2012, Oncogenic beta-catenin triggers an inflammatory response that determines the aggressiveness of hepatocellular carcinoma in mice, J. Clin. Invest., 122, 586, 10.1172/JCI43937 · DOI
- Tang, 2022, Aberrant cholesterol metabolic signaling impairs antitumor immunosurveillance through natural killer T cell dysfunction in obese liver, Cell. Mol. Immunol., 19, 834, 10.1038/s41423-022-00872-3 · DOI
- Syn, 2010, Accumulation of natural killer T cells in progressive nonalcoholic fatty liver disease, Hepatology, 51, 1998, 10.1002/hep.23599 · DOI · Paper page
- Arrese, 2016, Innate immunity and inflammation in NAFLD/NASH, Dig. Dis. Sci., 61, 1294, 10.1007/s10620-016-4049-x · DOI
- Hirsova, 2021, Emerging roles of T cells in the pathogenesis of nonalcoholic steatohepatitis and hepatocellular carcinoma, Front. Endocrinol., 12, 10.3389/fendo.2021.760860 · DOI
- Gao, 2016, Inflammation in alcoholic and nonalcoholic fatty liver disease: friend or foe?, Gastroenterology, 150, 1704, 10.1053/j.gastro.2016.01.025 · DOI
- Chen, 2022, Role of innate lymphoid cells in obesity and insulin resistance, Front. Endocrinol., 13
- Brestoff, 2015, Group 2 innate lymphoid cells promote beiging of white adipose tissue and limit obesity, Nature, 519, 242, 10.1038/nature14115 · DOI · Paper page
- Eberl, 2015, Innate lymphoid cells. Innate lymphoid cells: a new paradigm in immunology, Science, 348, aaa6566, 10.1126/science.aaa6566 · DOI · Paper page
- Dusseaux, 2011, Human MAIT cells are xenobiotic-resistant, tissue-targeted, CD161hi IL-17-secreting T cells, Blood, 117, 1250, 10.1182/blood-2010-08-303339 · DOI
- Toubal, 2020, Mucosal-associated invariant T cells promote inflammation and intestinal dysbiosis leading to metabolic dysfunction during obesity, Nat. Commun., 11, 3755, 10.1038/s41467-020-17307-0 · DOI · Paper page
- Tosello-Trampont, 2016, NKp46(+) natural killer cells attenuate metabolism-induced hepatic fibrosis by regulating macrophage activation in mice, Hepatology, 63, 799, 10.1002/hep.28389 · DOI · Paper page
- Gonzalez-Polo, 2019, Group 2 innate lymphoid cells exhibit progressively higher levels of activation during worsening of liver fibrosis, Ann. Hepatol., 18, 366, 10.1016/j.aohep.2018.12.001 · DOI
- Xu, 2021, Group-2 innate lymphoid cells promote HCC progression through CXCL2-neutrophil-induced immunosuppression, Hepatology, 74, 2526, 10.1002/hep.31855 · DOI
- Li, 2018, Mucosal-associated invariant T cells improve nonalcoholic fatty liver disease through regulating macrophage polarization, Front. Immunol., 9, 1994, 10.3389/fimmu.2018.01994 · DOI · Paper page
- Hegde, 2018, Mucosal-associated invariant T cells are a profibrogenic immune cell population in the liver, Nat. Commun., 9, 2146, 10.1038/s41467-018-04450-y · DOI · Paper page
- Corbett, 2020, Antigen recognition by MR1-reactive T cells; MAIT cells, metabolites, and remaining mysteries, Front. Immunol., 11, 1961, 10.3389/fimmu.2020.01961 · DOI
- Shuai, 2016, Adaptive immunity in the liver, Cell. Mol. Immunol., 13, 354, 10.1038/cmi.2016.4 · DOI
- Sanz, 2019, Challenges and opportunities for consistent classification of human B cell and plasma cell populations, Front. Immunol., 10, 2458, 10.3389/fimmu.2019.02458 · DOI · Paper page
- Raphael, 2015, T cell subsets and their signature cytokines in autoimmune and inflammatory diseases, Cytokine, 74, 5, 10.1016/j.cyto.2014.09.011 · DOI
- Moreno-Fernandez, 2021, PKM2-dependent metabolic skewing of hepatic Th17 cells regulates pathogenesis of non-alcoholic fatty liver disease, Cell Metab., 33, 1187, 10.1016/j.cmet.2021.04.018 · DOI
- Kremer, 2006, Favored T helper 1 response in a mouse model of hepatosteatosis is associated with enhanced T cell-mediated hepatitis, Hepatology, 44, 216, 10.1002/hep.21221 · DOI
- Chackelevicius, 2016, Th17 involvement in nonalcoholic fatty liver disease progression to non-alcoholic steatohepatitis, World J. Gastroenterol., 22, 9096, 10.3748/wjg.v22.i41.9096 · DOI
- Gomes, 2016, Metabolic inflammation-associated IL-17A causes non-alcoholic steatohepatitis and hepatocellular carcinoma, Cancer Cell, 30, 161, 10.1016/j.ccell.2016.05.020 · DOI · Paper page
- Harley, 2014, IL-17 signaling accelerates the progression of nonalcoholic fatty liver disease in mice, Hepatology, 59, 1830, 10.1002/hep.26746 · DOI
- Tang, 2011, Interleukin-17 exacerbates hepatic steatosis and inflammation in non-alcoholic fatty liver disease, Clin. Exp. Immunol., 166, 281, 10.1111/j.1365-2249.2011.04471.x · DOI · Paper page
- Rai, 2020, Blocking integrin alpha(4)beta(7)-mediated CD4 T cell recruitment to the intestine and liver protects mice from western diet-induced non-alcoholic steatohepatitis, J. Hepatol., 73, 1013, 10.1016/j.jhep.2020.05.047 · DOI · Paper page
- Ferreyra Solari, 2012, The role of innate cells is coupled to a Th1-polarized immune response in pediatric nonalcoholic steatohepatitis, J. Clin. Immunol., 32, 611, 10.1007/s10875-011-9635-2 · DOI
- Luo, 2013, IFN-gamma deficiency attenuates hepatic inflammation and fibrosis in a steatohepatitis model induced by a methionine- and choline-deficient high-fat diet, Am. J. Physiol. Gastrointest. Liver Physiol., 305, G891, 10.1152/ajpgi.00193.2013 · DOI · Paper page
- Meng, 2012, Interleukin-17 signaling in inflammatory, Kupffer cells, and hepatic stellate cells exacerbates liver fibrosis in mice, Gastroenterology, 143, 765, 10.1053/j.gastro.2012.05.049 · DOI · Paper page
- Tan, 2013, IL-17A plays a critical role in the pathogenesis of liver fibrosis through hepatic stellate cell activation, J. Immunol., 191, 1835, 10.4049/jimmunol.1203013 · DOI
- He, 2017, The imbalance of Th17/Treg cells is involved in the progression of nonalcoholic fatty liver disease in mice, BMC Immunol., 18, 33, 10.1186/s12865-017-0215-y · DOI
- Ma, 2007, A high-fat diet and regulatory T cells influence susceptibility to endotoxin-induced liver injury, Hepatology, 46, 1519, 10.1002/hep.21823 · DOI
- Wang, 2021, Bone marrow adipocytes: a critical player in the bone marrow microenvironment, Front. Cell Dev. Biol., 9
- Söderberg, 2011, Microvesicular fat, inter cellular adhesion molecule-1 and regulatory T-lymphocytes are of importance for the inflammatory process in livers with non-alcoholic steatohepatitis, APMIS, 119, 412, 10.1111/j.1600-0463.2011.02746.x · DOI
- Bhattacharjee, 2017, Hepatic natural killer T-cell and CD8+ T-cell signatures in mice with nonalcoholic steatohepatitis, Hepatol. Commun., 1, 299, 10.1002/hep4.1041 · DOI · Paper page
- Wabitsch, 2022, Metformin treatment rescues CD8(+) T-cell response to immune checkpoint inhibitor therapy in mice with NAFLD, J. Hepatol., 77, 748, 10.1016/j.jhep.2022.03.010 · DOI
- Koda, 2021, CD8(+) tissue-resident memory T cells promote liver fibrosis resolution by inducing apoptosis of hepatic stellate cells, Nat. Commun., 12, 4474, 10.1038/s41467-021-24734-0 · DOI · Paper page
- McVey, 2022, NAFLD indirectly impairs antigen-specific CD8(+) T cell immunity against liver cancer in mice, iScience, 25, 10.1016/j.isci.2022.103847 · DOI
- Barrow, 2021, The emerging role of B cells in the pathogenesis of NAFLD, Hepatology, 74, 2277, 10.1002/hep.31889 · DOI · Paper page
- Zhang, 2016, Role of intrahepatic B cells in non-alcoholic fatty liver disease by secreting pro-inflammatory cytokines and regulating intrahepatic T cells, J. Dig. Dis., 17, 464, 10.1111/1751-2980.12362 · DOI · Paper page
- McPherson, 2014, Serum immunoglobulin levels predict fibrosis in patients with non-alcoholic fatty liver disease, J. Hepatol., 60, 1055, 10.1016/j.jhep.2014.01.010 · DOI · Paper page
- Albano, 2005, Immune response towards lipid peroxidation products as a predictor of progression of non-alcoholic fatty liver disease to advanced fibrosis, Gut, 54, 987, 10.1136/gut.2004.057968 · DOI · Paper page
- Nobili, 2010, Oxidative stress parameters in paediatric non-alcoholic fatty liver disease, Int. J. Mol. Med., 26, 471, 10.3892/ijmm_00000487 · DOI
- McDaniel, 2021, Innate control of adaptive immunity and adaptive instruction of innate immunity: bi-directional flow of information, Curr. Opin. Immunol., 73, 25, 10.1016/j.coi.2021.07.013 · DOI
- Poggi, 2015, CD28 deletion improves obesity-induced liver steatosis but increases adiposity in mice, Int. J. Obes., 39, 977, 10.1038/ijo.2015.26 · DOI
- Chatzigeorgiou, 2014, Dual role of B7 costimulation in obesity-related nonalcoholic steatohepatitis and metabolic dysregulation, Hepatology, 60, 1196, 10.1002/hep.27233 · DOI
- Kim, 2011, Deficiency for costimulatory receptor 4-1BB protects against obesity-induced inflammation and metabolic disorders, Diabetes, 60, 3159, 10.2337/db10-1805 · DOI
- Sun, 2018, OX40 regulates both innate and adaptive immunity and promotes nonalcoholic steatohepatitis, Cell Rep., 25, 3786, 10.1016/j.celrep.2018.12.006 · DOI
- Guo, 2013, CD40 deficiency in mice exacerbates obesity-induced adipose tissue inflammation, hepatic steatosis, and insulin resistance, Am. J. Physiol. Endocrinol. Metab., 304, E951, 10.1152/ajpendo.00514.2012 · DOI
- Wolf, 2014, Coinhibitory suppression of T cell activation by CD40 protects against obesity and adipose tissue inflammation in mice, Circulation, 129, 2414, 10.1161/CIRCULATIONAHA.113.008055 · DOI
- Aarts, 2019, Depletion of CD40 on CD11c+ cells worsens the metabolic syndrome and ameliorates hepatic inflammation during NASH, Sci. Rep., 9, 10.1038/s41598-019-50976-6 · DOI
- Wolf, 2012, CD40L deficiency attenuates diet-induced adipose tissue inflammation by impairing immune cell accumulation and production of pathogenic IgG-antibodies, PLoS One, 7, 10.1371/annotation/84102aae-770a-41ae-9c15-4736ed129c17 · DOI
- Poggi, 2011, CD40L deficiency ameliorates adipose tissue inflammation and metabolic manifestations of obesity in mice, Arterioscler. Thromb. Vasc. Biol., 31, 2251, 10.1161/ATVBAHA.111.231357 · DOI
- Villeneuve, 2010, A protective role for CD154 in hepatic steatosis in mice, Hepatology, 52, 1968, 10.1002/hep.23935 · DOI
- Item, 2017, Fas cell surface death receptor controls hepatic lipid metabolism by regulating mitochondrial function, Nat. Commun., 8, 480, 10.1038/s41467-017-00566-9 · DOI
- Wieser, 2018, Adipose type I interferon signalling protects against metabolic dysfunction, Gut, 67, 157, 10.1136/gutjnl-2016-313155 · DOI
- Wang, 2014, Interferon regulatory factor 3 constrains IKKbeta/NF-kappaB signaling to alleviate hepatic steatosis and insulin resistance, Hepatology, 59, 870, 10.1002/hep.26751 · DOI
- Alzaid, 2016, IRF5 governs liver macrophage activation that promotes hepatic fibrosis in mice and humans, JCI Insight, 1, 10.1172/jci.insight.88689 · DOI
- Wang, 2013, Interferon regulatory factor 9 protects against hepatic insulin resistance and steatosis in male mice, Hepatology, 58, 603, 10.1002/hep.26368 · DOI
- Chan, 2021, A BAFF/APRIL axis regulates obesogenic diet-driven weight gain, Nat. Commun., 12, 2911, 10.1038/s41467-021-23084-1 · DOI
- Yamaguchi, 2010, Blockade of interleukin-6 signaling enhances hepatic steatosis but improves liver injury in methionine choline-deficient diet-fed mice, Lab. Invest., 90, 1169, 10.1038/labinvest.2010.75 · DOI
- Unutmaz, 1994, Antigen-independent activation of naive and memory resting T cells by a cytokine combination, J. Exp. Med., 180, 1159, 10.1084/jem.180.3.1159 · DOI
- Geginat, 2002, TCR-independent proliferation and differentiation of human CD4+ T cell subsets induced by cytokines, Adv. Exp. Med. Biol., 512, 107, 10.1007/978-1-4615-0757-4_14 · DOI
- Saito, 2010, Dynamic regulation of T cell activation and co-stimulation through TCR-microclusters, FEBS Lett., 584, 4865, 10.1016/j.febslet.2010.11.036 · DOI
- Croft, 2009, The significance of OX40 and OX40L to T-cell biology and immune disease, Immunol. Rev., 229, 173, 10.1111/j.1600-065X.2009.00766.x · DOI
- Vinay, 1998, Role of 4-1BB in immune responses, Semin. Immunol., 10, 481, 10.1006/smim.1998.0157 · DOI
- Elgueta, 2009, Molecular mechanism and function of CD40/CD40L engagement in the immune system, Immunol. Rev., 229, 152, 10.1111/j.1600-065X.2009.00782.x · DOI
- Schwarz, 2005, Biological activities of reverse signal transduction through CD137 ligand, J. Leukoc. Biol., 77, 281, 10.1189/jlb.0904558 · DOI
- Sun, 2007, A new class of reverse signaling costimulators belongs to the TNF family, J. Immunol., 179, 4307, 10.4049/jimmunol.179.7.4307 · DOI
- Croft, 2010, Control of immunity by the TNFR-related molecule OX40 (CD134), Annu. Rev. Immunol., 28, 57, 10.1146/annurev-immunol-030409-101243 · DOI
- Orabona, 2004, CD28 induces immunostimulatory signals in dendritic cells via CD80 and CD86, Nat. Immunol., 5, 1134, 10.1038/ni1124 · DOI
- Utley, 2020, CD28 regulates metabolic fitness for long-lived plasma cell survival, Cell Rep., 31, 10.1016/j.celrep.2020.107815 · DOI
- Venuprasad, 2003, CD28 signaling in neutrophil induces T-cell chemotactic factor(s) modulating T-cell response, Hum. Immunol., 64, 38, 10.1016/S0198-8859(02)00689-4 · DOI
- Venuprasad, 2001, Immunobiology of CD28 expression on human neutrophils. I. CD28 regulates neutrophil migration by modulating CXCR-1 expression, Eur. J. Immunol., 31, 1536, 10.1002/1521-4141(200105)31:5<1536::AID-IMMU1536>3.0.CO;2-8 · DOI
- Zheng, 2008, Modulation of NKT cell development by B7-CD28 interaction: an expanding horizon for costimulation, PLoS One, 3, 10.1371/journal.pone.0002703 · DOI
- Woerly, 1999, Expression of CD28 and CD86 by human eosinophils and role in the secretion of type 1 cytokines (interleukin 2 and interferon gamma): inhibition by immunoglobulin A complexes, J. Exp. Med., 190, 487, 10.1084/jem.190.4.487 · DOI
- Sharpe, 2002, The B7-CD28 superfamily, Nat. Rev. Immunol., 2, 116, 10.1038/nri727 · DOI
- Ursini, 2012, Improvement in insulin resistance after short-term treatment with abatacept: case report and short review, Clin. Rheumatol., 31, 1401, 10.1007/s10067-012-2034-0 · DOI
- Kwon, 1989, cDNA sequences of two inducible T-cell genes, Proc. Natl. Acad. Sci. USA, 86, 1963, 10.1073/pnas.86.6.1963 · DOI
- Vinay, 2011, 4-1BB signaling beyond T cells, Cell. Mol. Immunol., 8, 281, 10.1038/cmi.2010.82 · DOI
- Kim, 2008, 4-1BB engagement costimulates NKT cell activation and exacerbates NKT cell ligand-induced airway hyperresponsiveness and inflammation, J. Immunol., 180, 2062, 10.4049/jimmunol.180.4.2062 · DOI
- Lee, 2019, Reverse signaling of tumor necrosis factor superfamily proteins in macrophages and microglia: superfamily portrait in the neuroimmune interface, Front. Immunol., 10, 262, 10.3389/fimmu.2019.00262 · DOI
- Eissner, 2004, Ligands working as receptors: reverse signaling by members of the TNF superfamily enhance the plasticity of the immune system, Cytokine Growth Factor Rev., 15, 353, 10.1016/j.cytogfr.2004.03.011 · DOI
- Eun, 2015, 4-1BB ligand signaling to T cells limits T cell activation, J. Immunol., 194, 134, 10.4049/jimmunol.1401383 · DOI
- Kim, 2020, 4-1BB delineates distinct activation status of exhausted tumor-infiltrating CD8(+) T cells in hepatocellular carcinoma, Hepatology, 71, 955, 10.1002/hep.30881 · DOI
- Paterson, 1987, Antigens of activated rat T lymphocytes including a molecule of 50,000 Mr detected only on CD4 positive T blasts, Mol. Immunol., 24, 1281, 10.1016/0161-5890(87)90122-2 · DOI
- Wang, 2004, Characterization and functional study of five novel monoclonal antibodies against human OX40L highlight reverse signalling: enhancement of IgG production of B cells and promotion of maturation of DCs, Tissue Antigens, 64, 566, 10.1111/j.1399-0039.2004.00300.x · DOI
- Soroosh, 2006, OX40-OX40 ligand interaction through T cell-T cell contact contributes to CD4 T cell longevity, J. Immunol., 176, 5975, 10.4049/jimmunol.176.10.5975 · DOI
- Bretscher, 1999, A two-step, two-signal model for the primary activation of precursor helper T cells, Proc. Natl. Acad. Sci. USA, 96, 185, 10.1073/pnas.96.1.185 · DOI
- Blair, 2000, CD40 ligand (CD154) triggers a short-term CD4(+) T cell activation response that results in secretion of immunomodulatory cytokines and apoptosis, J. Exp. Med., 191, 651, 10.1084/jem.191.4.651 · DOI
- Peng, 1996, Accessory signaling by CD40 for T cell activation: induction of Th1 and Th2 cytokines and synergy with interleukin-12 for interferon-gamma production, Eur. J. Immunol., 26, 1621, 10.1002/eji.1830260732 · DOI
- Lepreux, 2017, CD40 signaling and hepatic steatosis: unanticipated links, Clin. Res. Hepatol. Gastroenterol., 41, 357, 10.1016/j.clinre.2016.11.002 · DOI
- Takada, 2019, Integrin binding to the trimeric interface of CD40L plays a critical role in CD40/CD40L signaling, J. Immunol., 203, 1383, 10.4049/jimmunol.1801630 · DOI
- Peter, 2003, The CD95(APO-1/Fas) DISC and beyond, Cell Death Differ., 10, 26, 10.1038/sj.cdd.4401186 · DOI
- Suzuki, 1998, Maximal proliferation of cytotoxic T lymphocytes requires reverse signaling through Fas ligand, J. Exp. Med., 187, 123, 10.1084/jem.187.1.123 · DOI
- Boursalian, 2003, Mutation in fas ligand impairs maturation of thymocytes bearing moderate affinity T cell receptors, J. Exp. Med., 198, 349, 10.1084/jem.20030220 · DOI
- Isayama, 2016, Fas regulates macrophage polarization and fibrogenic phenotype in a model of chronic ethanol-induced hepatocellular injury, Am. J. Pathol., 186, 1524, 10.1016/j.ajpath.2016.02.006 · DOI
- Ottonello, 1999, Soluble Fas ligand is chemotactic for human neutrophilic polymorphonuclear leukocytes, J. Immunol., 162, 3601, 10.4049/jimmunol.162.6.3601 · DOI
- Hao, 2008, Fas receptor expression in germinal-center B cells is essential for T and B lymphocyte homeostasis, Immunity, 29, 615, 10.1016/j.immuni.2008.07.016 · DOI
- Alkhouri, 2015, Circulating soluble Fas and Fas ligand levels are elevated in children with nonalcoholic steatohepatitis, Dig. Dis. Sci., 60, 2353, 10.1007/s10620-015-3614-z · DOI
- Feldstein, 2003, Hepatocyte apoptosis and Fas expression are prominent features of human nonalcoholic steatohepatitis, Gastroenterology, 125, 437, 10.1016/S0016-5085(03)00907-7 · DOI · Paper page
- Crampton, 2010, Innate pathways to B-cell activation and tolerance, Ann. N. Y. Acad. Sci., 1183, 58, 10.1111/j.1749-6632.2009.05123.x · DOI
- Crouse, 2015, Regulation of antiviral T cell responses by type I interferons, Nat. Rev. Immunol., 15, 231, 10.1038/nri3806 · DOI
- Kiefer, 2012, Role of type I interferons in the activation of autoreactive B cells, Immunol. Cell Biol., 90, 498, 10.1038/icb.2012.10 · DOI
- Zhang, 2021, Type I interferon signaling mediates Mycobacterium tuberculosis-induced macrophage death, J. Exp. Med., 218, 10.1084/jem.20200887 · DOI
- Paolini, 2015, NK cells and interferons, Cytokine Growth Factor Rev., 26, 113, 10.1016/j.cytogfr.2014.11.003 · DOI
- Bekeredjian-Ding, 2005, Plasmacytoid dendritic cells control TLR7 sensitivity of naive B cells via type I IFN, J. Immunol., 174, 4043, 10.4049/jimmunol.174.7.4043 · DOI
- Akkaya, 2017, B cells produce type 1 IFNs in response to the TLR9 agonist CpG-A conjugated to cationic lipids, J. Immunol., 199, 931, 10.4049/jimmunol.1700348 · DOI
- Asselin-Paturel, 2005, Type I interferon dependence of plasmacytoid dendritic cell activation and migration, J. Exp. Med., 201, 1157, 10.1084/jem.20041930 · DOI
- Kim, 2016, Toll-like receptor 7 affects the pathogenesis of non-alcoholic fatty liver disease, Sci. Rep., 6
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Metadata
- Authors
- Sawada, K., Chung, H., Softic, S., Moreno-Fernandez, M. E., & Divanovic, S.
- Affiliations
- Cincinnati Children's Hospital Medical Center (US)
- University of Kentucky (US)
- Corresponding author
- Divanovic, Senad
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2023-11
- Volume
- 35
- Issue
- 11
- Pages
- 1852-1871
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC10680147
- OpenAlex
- W4388452323
- Cited by
- 139
- References
- 316
- Citations by year
- 2026: 56 · 2025: 51 · 2024: 32
- FWCI
- 5.43
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- American Heart Association (17POST33650045)
- CCHMC
- Cincinnati Children’s Research Foundation
- National Institutes of Health (R01DK099222)
- U.S. Department of Defense (W81XWH2010392)
- American Diabetes Association (1-18-IBS-100)
- Topics
- Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
- Keywords
- non-alcoholic fatty liver disease, innate immunity, adaptive immunity, liver inflammation, immune cell types, therapeutic target
- MeSH terms
- Fatty Liver, Humans, Inflammation, Metabolic Diseases, Pancreas, Risk Factors
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