Liver damage promotes pro-inflammatory T-cell responses against apolipoprotein B-100.


Journal

Journal of internal medicine
ISSN: 1365-2796
Titre abrégé: J Intern Med
Pays: England
ID NLM: 8904841

Informations de publication

Date de publication:
05 2022
Historique:
pubmed: 17 12 2021
medline: 15 4 2022
entrez: 16 12 2021
Statut: ppublish

Résumé

Liver-derived apolipoprotein B-100 (ApoB100) is an autoantigen that is recognized by atherogenic CD4 We identified ApoB100-specific T cells in blood from healthy controls, nonalcoholic fatty liver disease (NAFLD) patients, and CVD patients by activation-induced marker expression and analyzed their differentiation pattern in correlation to the lipid profile and liver damage parameters in a cross-sectional study. To assess the induction of extrahepatic ApoB100-specific T cells upon transient liver damage in vivo, we performed hydrodynamic tail vein injections with diphtheria toxin A (DTA)-encoding plasmid in human ApoB100-transgenic mice. Utilizing immunodominant ApoB100-derived peptides, we found increased ApoB100-specific T-cell populations in NAFLD and CVD patients compared to healthy controls. In a peptide-specific manner, ApoB100 reactivity in healthy controls was accompanied by expression of the regulatory T (Treg)-cell transcription factor FOXP3. In contrast, FOXP3 expression decreased, whereas expression of pro-inflammatory cytokine interleukin (IL)-17A increased in ApoB100-specific T cells from NAFLD and CVD patients. Dyslipidemia and liver damage parameters in blood correlated with reduced FOXP3 expression and elevated IL-17A production in ApoB100-specific T-cell populations, respectively. Moreover, DTA-mediated transient liver damage in human ApoB100-transgenic mice accumulated IL-17a-expressing ApoB100-specific T cells in the periphery. Our results show that liver damage promotes pro-inflammatory ApoB100-specific T-cell populations, thereby providing a cellular mechanism for the increased CVD risk in liver disease patients.

Identifiants

pubmed: 34914849
doi: 10.1111/joim.13434
doi:

Substances chimiques

Apolipoprotein B-100 0
Forkhead Transcription Factors 0
Interleukin-17 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

648-664

Informations de copyright

© 2021 The Authors. Journal of Internal Medicine published by John Wiley & Sons Ltd on behalf of Association for Publication of The Journal of Internal Medicine.

Références

Collaborators GBDCoD. Global, regional, and national age-sex-specific mortality for 282 causes of death in 195 countries and territories, 1980-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet. 2018;392:1736-88.
Cai J, Zhang X-J, Ji Y-X, Zhang P, She Z-G, Li H. Nonalcoholic fatty liver disease pandemic fuels the upsurge in cardiovascular diseases. Circ Res. 2020;126:679-704.
Kubes P, Jenne C. Immune responses in the liver. Annu Rev Immunol. 2018;36:247-77.
Petta S, Maida M, Macaluso FS, Barbara M, Licata A, Craxì A, et al. Hepatitis C virus infection is associated with increased cardiovascular mortality: a meta-analysis of observational studies. Gastroenterology. 2016;150:145-55.e4.
Stoll LL, Denning GM, Weintraub NL. Potential role of endotoxin as a proinflammatory mediator of atherosclerosis. Arterioscler Thromb Vasc Biol. 2004;24:2227-36.
Rehm J, Shield KD, Roerecke M, Gmel G. Modelling the impact of alcohol consumption on cardiovascular disease mortality for comparative risk assessments: an overview. BMC Public Health. 2016;16:363.
Ostos MA, Recalde D, Zakin MM, Scott-Algara D. Implication of natural killer T cells in atherosclerosis development during a LPS-induced chronic inflammation. FEBS Lett. 2002;519:23-9.
Luchtefeld M, Schunkert H, Stoll M, Selle T, Lorier R, Grote K, et al. Signal transducer of inflammation gp130 modulates atherosclerosis in mice and man. J Exp Med. 2007;204:1935-44.
Defilippis AP, Blaha MJ, Martin SS, Reed RM, Jones SR, Nasir K, et al. Nonalcoholic fatty liver disease and serum lipoproteins: the Multi-Ethnic Study of Atherosclerosis. Atherosclerosis. 2013;227:429-36.
Ridker PM, Everett BM, Thuren T, Macfadyen JG, Chang WH, Ballantyne C, et al. Antiinflammatory therapy with canakinumab for atherosclerotic disease. N Engl J Med. 2017;377:1119-31.
Tabas I, Williams KJ, Borén J. Subendothelial lipoprotein retention as the initiating process in atherosclerosis: update and therapeutic implications. Circulation. 2007;116:1832-44.
Stemme S, Faber B, Holm J, Wiklund O, Witztum JL, Hansson GK. T lymphocytes from human atherosclerotic plaques recognize oxidized low density lipoprotein. Proc Natl Acad Sci U S A. 1995;92:3893-7.
Gisterå A, Klement ML, Polyzos KA, Mailer RKW, Duhlin A, Karlsson MCI, et al. Low-density lipoprotein-reactive T cells regulate plasma cholesterol levels and development of atherosclerosis in humanized hypercholesterolemic mice. Circulation. 2018;138:2513-26.
Kimura T, Kobiyama K, Winkels H, Tse K, Miller J, Vassallo M, et al. Regulatory CD4(+) T cells recognize major histocompatibility complex class II molecule-restricted peptide epitopes of apolipoprotein B. Circulation. 2018;138:1130-43.
Gisterå A, Hermansson A, Strodthoff D, Klement ML, Hedin U, Fredrikson GN, et al. Vaccination against T-cell epitopes of native ApoB100 reduces vascular inflammation and disease in a humanized mouse model of atherosclerosis. J Intern Med. 2017;281:383-97.
Wolf D, Ley K. Immunity and Inflammation in Atherosclerosis. Circ Res. 2019;124:315-27.
Van Herck MA, Weyler J, Kwanten WJ, Dirinck EL, De Winter BY, Francque SM, et al. The differential roles of T cells in non-alcoholic fatty liver disease and obesity. Front Immunol. 2019;10:82.
Frostegård J, Ulfgren A-K, Nyberg P, Hedin U, Swedenborg J, Andersson U, et al. Cytokine expression in advanced human atherosclerotic plaques: dominance of pro-inflammatory (Th1) and macrophage-stimulating cytokines. Atherosclerosis. 1999;145:33-43.
Erbel C, Dengler TJ, Wangler S, Lasitschka F, Bea F, Wambsganss N, et al. Expression of IL-17A in human atherosclerotic lesions is associated with increased inflammation and plaque vulnerability. Basic Res Cardiol. 2011;106:125-34.
Tang Y, Bian Z, Zhao L, Liu Y, Liang S, Wang Q, et al. Interleukin-17 exacerbates hepatic steatosis and inflammation in non-alcoholic fatty liver disease. Clin Exp Immunol. 2011;166:281-90.
Rau M, Schilling A-K, Meertens J, Hering I, Weiss J, Jurowich C, et al. Progression from nonalcoholic fatty liver to nonalcoholic steatohepatitis is marked by a higher frequency of Th17 cells in the liver and an increased Th17/Resting regulatory T cell ratio in peripheral blood and in the liver. J Immunol. 2016;196:97-105.
Kremer M, Hines IN, Milton RJ, Wheeler MD. Favored T helper 1 response in a mouse model of hepatosteatosis is associated with enhanced T cell-mediated hepatitis. Hepatology. 2006;44:216-27.
Gisterå A, Robertson A-KL, Andersson J, Ketelhuth DFJ, Ovchinnikova O, Nilsson SK, et al. Transforming growth factor-beta signaling in T cells promotes stabilization of atherosclerotic plaques through an interleukin-17-dependent pathway. Sci Transl Med. 2013;5:196ra00.
Simon T, Taleb S, Danchin N, Laurans L, Rousseau B, Cattan S, et al. Circulating levels of interleukin-17 and cardiovascular outcomes in patients with acute myocardial infarction. Eur Heart J. 2013;34:570-7.
Mailer RKW, Joly A-L, Liu S, Elias S, Tegner J, Andersson J. IL-1beta promotes Th17 differentiation by inducing alternative splicing of FOXP3. Sci Rep. 2015;5:14674.
Mailer RKW, Gisterå A, Polyzos KA, Ketelhuth DFJ, Hansson GK. Hypercholesterolemia induces differentiation of regulatory T cells in the liver. Circ Res. 2017;120:1740-53.
Wolf D, Gerhardt T, Winkels H, Michel NA, Pramod AB, Ghosheh Y, et al. Pathogenic autoimmunity in atherosclerosis evolves from initially protective apolipoprotein B100-reactive CD4(+) T-regulatory cells. Circulation. 2020;142:1279-93.
Luth S, Huber S, Schramm C, Buch T, Zander S, Stadelmann C, et al. Ectopic expression of neural autoantigen in mouse liver suppresses experimental autoimmune neuroinflammation by inducing antigen-specific Tregs. J Clin Invest. 2008;118:3403-10.
Frentsch M, Arbach O, Kirchhoff D, Moewes B, Worm M, Rothe M, et al. Direct access to CD4+ T cells specific for defined antigens according to CD154 expression. Nat Med. 2005;11:1118-24.
Litjens NHR, Boer K, Betjes MGH. Identification of circulating human antigen-reactive CD4+ FOXP3+ natural regulatory T cells. J Immunol. 2012;188:1083-90.
Mailer RKW. Alternative splicing of FOXP3-virtue and vice. Front Immunol. 2018;9:530.
Wang P, Sidney J, Kim Y, Sette A, Lund O, Nielsen M, et al. Peptide binding predictions for HLA DR, DP and DQ molecules. BMC Bioinformatics. 2010;11:568.
Stindt J, Kluge S, Dröge C, Keitel V, Stross C, Baumann U, et al. Bile salt export pump-reactive antibodies form a polyclonal, multi-inhibitory response in antibody-induced bile salt export pump deficiency. Hepatology. 2016;63:524-37.
Okushin K, Tsutsumi T, Enooku K, Fujinaga H, Kado A, Shibahara J, et al. The intrahepatic expression levels of bile acid transporters are inversely correlated with the histological progression of nonalcoholic fatty liver disease. J Gastroenterol. 2016;51:808-18.
Ramachandran P, Dobie R, Wilson-Kanamori JR, Dora EF, Henderson BEP, Luu NT, et al. Resolving the fibrotic niche of human liver cirrhosis at single-cell level. Nature. 2019;575:512-8.
Cai J, Zhang X-J, Li H. Role of innate immune signaling in non-alcoholic fatty liver disease. Trends Endocrinol Metab. 2018;29:712-22.
Chan AT, Manson JE, Albert CM, Chae CU, Rexrode KM, Curhan GC, et al. Nonsteroidal antiinflammatory drugs, acetaminophen, and the risk of cardiovascular events. Circulation. 2006;113:1578-87.
Cheng X, Yu X, Ding Y-J, Fu Q-Q, Xie J-J, Tang T-T, et al. The Th17/Treg imbalance in patients with acute coronary syndrome. Clin Immunol. 2008;127:89-97.
Chan DC, Watts GF, Gan S, Wong ATY, Ooi EMM, Barrett PHR. Nonalcoholic fatty liver disease as the transducer of hepatic oversecretion of very-low-density lipoprotein-apolipoprotein B-100 in obesity. Arterioscler Thromb Vasc Biol. 2010;30:1043-50.
Mailer RKW, Gisterå A, Polyzos KA, Ketelhuth DFJ, Hansson GK. Hypercholesterolemia enhances T cell receptor signaling and increases the regulatory T cell population. Sci Rep. 2017;7:15655.
Lundberg AK, Jonasson L, Hansson GK, Mailer RKW. Activation-induced FOXP3 isoform profile in peripheral CD4+ T cells is associated with coronary artery disease. Atherosclerosis. 2017;267:27-33.
Proto JD, Doran AC, Subramanian M, Wang H, Zhang M, Sozen E, et al. Hypercholesterolemia induces T cell expansion in humanized immune mice. J Clin Invest. 2018;128:2370-5.
Herbin O, Ait-Oufella H, Yu W, Fredrikson GN, Aubier B, Perez N, et al. Regulatory T-cell response to apolipoprotein B100-derived peptides reduces the development and progression of atherosclerosis in mice. Arterioscler Thromb Vasc Biol. 2012;32:605-12.
Fredrikson GN, Björkbacka H, Söderberg I, Ljungcrantz I, Nilsson J. Treatment with apo B peptide vaccines inhibits atherosclerosis in human apo B-100 transgenic mice without inducing an increase in peptide-specific antibodies. J Intern Med. 2008;264:563-70.
Pike AF, Kramer NI, Blaauboer BJ, Seinen W, Brands R. A novel hypothesis for an alkaline phosphatase ‘rescue’ mechanism in the hepatic acute phase immune response. Biochim Biophys Acta. 2013;1832:2044-56.
Ioannou GN, Weiss NS, Boyko EJ, Mozaffarian D, Lee SP. Elevated serum alanine aminotransferase activity and calculated risk of coronary heart disease in the United States. Hepatology. 2006;43:1145-51.
Ekstedt M, Hagström H, Nasr P, Fredrikson M, Stål P, Kechagias S, et al. Fibrosis stage is the strongest predictor for disease-specific mortality in NAFLD after up to 33 years of follow-up. Hepatology. 2015;61:1547-54.
Rahman M, Steuer J, Gillgren P, Hayderi A, Liu A, Frostegård J. Induction of dendritic cell-mediated activation of T cells from atherosclerotic plaques by human heat shock protein 60. J Am Heart Assoc. 2017;6:e006778.
Lee SB, Park G-M, Lee J-Y, Lee B, Park JH, Kim BG, et al. Association between non-alcoholic fatty liver disease and subclinical coronary atherosclerosis: an observational cohort study. J Hepatol. 2018;68:1018-24.

Auteurs

Bastian F J Plochg (BFJ)

Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Hanna Englert (H)

Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Chandini Rangaswamy (C)

Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Sandra Konrath (S)

Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Mandy Malle (M)

Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Sibylle Lampalzer (S)

Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Claudia Beisel (C)

Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
German Center for Infection Research (DZIF), Partner Site Hamburg-Lübeck-Borstel-Riems, Hamburg, Germany.

Salma Wollin (S)

Medical Clinic and Polyclinic, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Section Endocrinology and Diabetology, University Obesity Centre Hamburg, University Hospital Hamburg-Eppendorf, Germany.

Maike Frye (M)

Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Jens Aberle (J)

Medical Clinic and Polyclinic, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Section Endocrinology and Diabetology, University Obesity Centre Hamburg, University Hospital Hamburg-Eppendorf, Germany.

Johannes Kluwe (J)

Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Thomas Renné (T)

Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Reiner K Mailer (RK)

Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

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