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Inflammation Research
Erschienen in: Inflammation Research 12/2022

25.10.2022 | Review

Immunosenescence of T cells: a key player in rheumatoid arthritis

verfasst von: Yi Gao, Weiwei Cai, Ying Zhou, Yuhui Li, Jingwen Cheng, Fang Wei

Erschienen in: Inflammation Research | Ausgabe 12/2022

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Abstract

Introduction

The incidence of rheumatoid arthritis (RA) and its complications are expected to increase with age. Remarkably, RA patients were identified features of accelerated aging, particularly in immunosenescence. As is known, T cells in RA patients readily differentiate into pro-inflammatory phenotypes that maintain chronic and persistent inflammatory changes in joints and many other organ systems. Recent evidence suggests that T cells are most sensitive to aging, and aged CD4+ T cells contribute to inflammaging, which plays a crucial role in accelerating the disease process. In recent years, the molecular mechanisms of T cell immunosenescence were beginning to be understood. Immune aging in RA T cells is associated with thymus insufficiency, metabolic abnormalities, shortened telomere length, and chronic energy stress. Therefore, we summarized the role and mechanism of T cell immunosenescence in RA.

Methods

A computer-based online search was performed using the PubMed database for published articles concerning T cells aging and rheumatoid arthritis.

Results

In this review, we assess the roles of CD4+ T cells in the center of inflammaging especially in RA and emphasize arthritogenic effector functions of senescent T cell; also we discuss the possible molecular mechanisms of senescent T cells and therapeutic targets to intervene T cells immunosenescence for improvement of RA.
Literatur
1.
Smolen, J.S., et al., Rheumatoid arthritis. Nature Reviews Disease Primers, 2018. 4(1).
2.
Weyand CM, Zeisbrich M, Goronzy JJ. Metabolic signatures of T-cells and macrophages in rheumatoid arthritis. Curr Opin Immunol. 2017;46:112–20.PubMedPubMedCentralCrossRef
3.
4.
Aletaha D, Smolen JS. Diagnosis and management of rheumatoid arthritis: a review. JAMA. 2018;320(13):1360–72.PubMedCrossRef
5.
McInnes IB, Schett G. Pathogenetic insights from the treatment of rheumatoid arthritis. The Lancet. 2017;389(10086):2328–37.CrossRef
6.
Dedmon LE. The genetics of rheumatoid arthritis. Rheumatol (Oxford). 2020;59(10):2661–70.CrossRef
7.
Amariuta T, et al. Advances in genetics toward identifying pathogenic cell states of rheumatoid arthritis. Immunol Rev. 2020;294(1):188–204.PubMedCrossRef
8.
9.
10.
11.
12.
Moro-Garcia MA, et al. Influence of inflammation in the process of T lymphocyte differentiation: proliferative, metabolic, and oxidative changes. Front Immunol. 2018;9:339.PubMedPubMedCentralCrossRef
13.
Nikolich-Zugich J. The twilight of immunity: emerging concepts in aging of the immune system. Nat Immunol. 2018;19(1):10–9.PubMedCrossRef
14.
Goh J et al. Targeting the molecular and cellular pillars of human aging with exercise. FEBS J. 2021
15.
16.
17.
18.
Gonzalez-Osuna L, et al. Premature senescence of T-cells favors bone loss during osteolytic diseases a new concern in the osteoimmunology arena. Aging Dis. 2021;12(5):1150–61.PubMedPubMedCentralCrossRef
19.
Sood A, Raji MA. Cognitive impairment in elderly patients with rheumatic disease and the effect of disease-modifying anti-rheumatic drugs. Clin Rheumatol. 2021;40(4):1221–31.PubMedCrossRef
20.
21.
Fessler J, Angiari S. The role of T cell senescence in neurological diseases and its regulation by cellular metabolism. Front Immunol. 2021;12: 706434.PubMedPubMedCentralCrossRef
22.
23.
24.
25.
Petersen LE, et al. Characterization of senescence biomarkers in rheumatoid arthritis: relevance to disease progression. Clin Rheumatol. 2019;38(10):2909–15.PubMedCrossRef
26.
27.
Plunkett FJ, et al. The loss of telomerase activity in highly differentiated CD8+CD28-CD27- T cells is associated with decreased Akt (Ser473) phosphorylation. J Immunol. 2007;178(12):7710–9.PubMedCrossRef
28.
29.
Fessler J, et al. Premature senescence of T-cell subsets in axial spondyloarthritis. Ann Rheum Dis. 2016;75(4):748–54.PubMedCrossRef
30.
Luque-Campos N, et al. Mesenchymal stem cells improve rheumatoid arthritis progression by controlling memory T cell response. Front Immunol. 2019;10:798.PubMedPubMedCentralCrossRef
31.
32.
33.
Wang Y, et al. Germline genetic patterns underlying familial rheumatoid arthritis, systemic lupus erythematosus and primary Sjogren’s syndrome highlight T cell-initiated autoimmunity. Ann Rheum Dis. 2020;79(2):268–75.PubMedCrossRef
34.
35.
36.
37.
van der Geest KSM, et al. Aging disturbs the balance between effector and regulatory CD4+ T cells. Exp Gerontol. 2014;60:190–6.PubMedCrossRef
38.
Chemin K, Gerstner C, Malmstrom V. Effector functions of CD4+ T cells at the site of local autoimmune inflammation-lessons from rheumatoid arthritis. Front Immunol. 2019;10:353.PubMedPubMedCentralCrossRef
39.
Ruterbusch M, et al. In vivo CD4(+) T cell differentiation and function: revisiting the Th1/Th2 paradigm. Annu Rev Immunol. 2020;38:705–25.PubMedCrossRef
40.
Schmitt V, Rink L, Uciechowski P. The Th17/Treg balance is disturbed during aging. Exp Gerontol. 2013;48(12):1379–86.PubMedCrossRef
41.
Kumar P, Bhattacharya P, Prabhakar BS. A comprehensive review on the role of co-signaling receptors and treg homeostasis in autoimmunity and tumor immunity. J Autoimmun. 2018;95:77–99.PubMedPubMedCentralCrossRef
42.
Bharath LP, et al. Metformin enhances autophagy and normalizes mitochondrial function to alleviate aging-associated inflammation. Cell Metab. 2020;32(1):44–55 (e6).PubMedPubMedCentralCrossRef
43.
44.
Ouyang X, et al. Potentiation of Th17 cytokines in aging process contributes to the development of colitis. Cell Immunol. 2011;266(2):208–17.PubMedCrossRef
45.
Lucas C, Perdriger A, Ame P. Definition of B cell helper T cells in rheumatoid arthritis and their behavior during treatment. Semin Arthritis Rheum. 2020;50(5):867–72.PubMedCrossRef
46.
47.
Kerola AM, et al. Incidence, sociodemographic factors and treatment penetration of rheumatoid arthritis and psoriatic arthritis in Norway. Semin Arthritis Rheum. 2021;51(5):1081–8.PubMedCrossRef
48.
49.
Lenaers G, et al. Dysfunctional T cell mitochondria lead to premature aging. Trends Mol Med. 2020;26(9):799–800.PubMedCrossRef
50.
Shao L, Goronzy JJ, Weyand CM. DNA-dependent protein kinase catalytic subunit mediates T-cell loss in rheumatoid arthritis. EMBO Mol Med. 2010;2(10):415–27.PubMedPubMedCentralCrossRef
51.
Costenbader KH, et al. Immunosenescence and rheumatoid arthritis: does telomere shortening predict impending disease? Autoimmun Rev. 2011;10(9):569–73.PubMedPubMedCentralCrossRef
52.
53.
Chavez MD, Tse HM. Targeting mitochondrial-derived reactive oxygen species in T cell-mediated autoimmune diseases. Front Immunol. 2021;12: 703972.PubMedPubMedCentralCrossRef
54.
Papadaki HA, et al. Bone marrow progenitor cell reserve and function and stromal cell function are defective in rheumatoid arthritis: evidence for a tumor necrosis factor alpha-mediated effect. Blood. 2002;99(5):1610–9.PubMedCrossRef
55.
Goronzy JJ, Weyand CM. Aging, autoimmunity and arthritis: T-cell senescence and contraction of T-cell repertoire diversity—catalysts of autoimmunity and chronic inflammation. Arthritis Res Ther. 2003;5(5):225–34.PubMedPubMedCentralCrossRef
56.
Li Z, Guo J, Bi L. Role of the NLRP3 inflammasome in autoimmune diseases. Biomed Pharmacother. 2020;130: 110542.PubMedCrossRef
57.
Patlán M, et al. Relative increase of Th17 phenotype in senescent CD4+CD28null T cells from peripheral blood of patients with rheumatoid arthritis. Clin Exp Rheumatol. 2021;39(4):925–6.PubMedCrossRef
58.
59.
60.
ElTanbouly MA, Noelle RJ. Rethinking peripheral T cell tolerance: checkpoints across a T cell’s journey. Nat Rev Immunol. 2021;21(4):257–67.PubMedCrossRef
61.
Darrigues J, van Meerwijk JPM, Romagnoli P. Age-dependent changes in regulatory t lymphocyte development and function: a mini-review. Gerontology. 2018;64(1):28–35.PubMedCrossRef
62.
63.
Wang T, et al. Regulatory T cells in rheumatoid arthritis showed increased plasticity toward Th17 but retained suppressive function in peripheral blood. Ann Rheum Dis. 2015;74(6):1293–301.PubMedCrossRef
64.
65.
Robbins PD, et al. Senolytic drugs: reducing senescent cell viability to extend health span. Annu Rev Pharmacol Toxicol. 2021;61:779–803.PubMedCrossRef
66.
Novais EJ, et al. Long-term treatment with senolytic drugs dasatinib and quercetin ameliorates age-dependent intervertebral disc degeneration in mice. Nat Commun. 2021;12(1):5213.PubMedPubMedCentralCrossRef
67.
68.
Mannick JB, et al. mTOR inhibition improves immune function in the elderly. Sci Transl Med. 2014;6(268):268ra179.PubMedCrossRef
69.
70.
Boothby IC, Cohen JN, Rosenblum MD. Regulatory T cells in skin injury: at the crossroads of tolerance and tissue repair. Sci Immunol. 2020;5(47):eaaz9631.PubMedPubMedCentralCrossRef
71.
Klose CS, Artis D. Innate lymphoid cells as regulators of immunity, inflammation and tissue homeostasis. Nat Immunol. 2016;17(7):765–74.PubMedCrossRef
72.
73.
74.
Pandya JM, et al. Circulating T helper and T regulatory subsets in untreated early rheumatoid arthritis and healthy control subjects. J Leukoc Biol. 2016;100(4):823–33.PubMedCrossRef
75.
76.
77.
Salminen A. Increased immunosuppression impairs tissue homeostasis with aging and age-related diseases. J Mol Med (Berl). 2021;99(1):1–20.CrossRef
78.
Chen Z, et al. Anti-inflammatory and immune-regulatory cytokines in rheumatoid arthritis. Nat Rev Rheumatol. 2019;15(1):9–17.PubMedCrossRef
79.
Fessler J, et al. Novel senescent regulatory T-cell subset with impaired suppressive function in rheumatoid arthritis. Front Immunol. 2017;8:300.PubMedPubMedCentralCrossRef
80.
Meyer A, et al. Kinase activity profiling reveals contribution of G-protein signaling modulator 2 deficiency to impaired regulatory T cell migration in rheumatoid arthritis. J Autoimmun. 2021;124:102726.PubMedCrossRef
81.
Corrado M, Pearce EL. Targeting memory T cell metabolism to improve immunity. J Clin Invest, 2022;132(1):e148546.
82.
Fardellone P, et al. Bone Loss, Osteoporosis, and Fractures in Patients with Rheumatoid Arthritis: A Review. J Clin Med. 2020;9(10):3361.PubMedCentralCrossRef
83.
Komatsu N et al. Plasma cells promote osteoclastogenesis and periarticular bone loss in autoimmune arthritis. J Clin Invest, 2021;131(6):e143060.
84.
85.
Cho SK, et al. Effectiveness of bazedoxifene in preventing glucocorticoid-induced bone loss in rheumatoid arthritis patients. Arthritis Res Ther. 2021;23(1):176.PubMedPubMedCentralCrossRef
86.
87.
Wang G, et al. Cycloastragenol attenuates osteoclastogenesis and bone loss by targeting RANKL-induced Nrf2/Keap1/ARE, NF-kappaB, calcium, and NFATc1 pathways. Front Pharmacol. 2021;12: 810322.PubMedCrossRef
88.
Zerbini CAF, et al. Biologic therapies and bone loss in rheumatoid arthritis. Osteoporos Int. 2017;28(2):429–46.PubMedCrossRef
89.
90.
Finzel S, et al. Comparison of the effects of tocilizumab monotherapy and adalimumab in combination with methotrexate on bone erosion repair in rheumatoid arthritis. Ann Rheum Dis. 2019;78(9):1186–91.PubMedCrossRef
91.
Adam S, et al. JAK inhibition increases bone mass in steady-state conditions and ameliorates pathological bone loss by stimulating osteoblast function. Sci Transl Med. 2020;12(530):eaay4447.PubMedCrossRef
92.
Shim JH, Stavre Z, Gravallese EM. Bone loss in rheumatoid arthritis: basic mechanisms and clinical implications. Calcif Tissue Int. 2018;102(5):533–46.PubMedCrossRef
93.
Cici D, et al. Wnt signaling and biological therapy in rheumatoid arthritis and spondyloarthritis. Int J Mol Sci. 2019;20(22):5552.PubMedCentralCrossRef
94.
Szentpetery A, et al. Effects of targeted therapies on the bone in arthritides. Autoimmun Rev. 2017;16(3):313–20.PubMedCrossRef
95.
Najm A, et al. MicroRNA-17-5p reduces inflammation and bone erosions in mice with collagen-induced arthritis and directly targets the JAK/STAT pathway in rheumatoid arthritis fibroblast-like synoviocytes. Arthritis Rheumatol. 2020;72(12):2030–9.PubMedCrossRef
96.
Bhadricha H, et al. Increased frequency of Th17 cells and IL-17 levels are associated with low bone mineral density in postmenopausal women. Sci Rep. 2021;11(1):16155.PubMedPubMedCentralCrossRef
97.
Blackford AN, Jackson SP. ATM, ATR, and DNA-PK: the trinity at the heart of the DNA damage response. Mol Cell. 2017;66(6):801–17.PubMedCrossRef
98.
Li Y, Goronzy JJ, Weyand CM. DNA damage, metabolism and aging in pro-inflammatory T cells: rheumatoid arthritis as a model system. Exp Gerontol. 2018;105:118–27.PubMedCrossRef
99.
100.
Ummarino D. Rheumatoid arthritis: DNA repair links T-cell ageing to inflammation. Nat Rev Rheumatol. 2016;12(12):694.PubMedCrossRef
101.
Li Y, et al. Deficient activity of the nuclease MRE11A induces T cell aging and promotes arthritogenic effector functions in patients with rheumatoid arthritis. Immunity. 2016;45(4):903–16.PubMedPubMedCentralCrossRef
102.
Wiley CD, et al. Mitochondrial dysfunction induces senescence with a distinct secretory phenotype. Cell Metab. 2016;23(2):303–14.PubMedCrossRef
103.
Li Y, et al. The DNA repair nuclease MRE11A functions as a mitochondrial protector and prevents T cell pyroptosis and tissue inflammation. Cell Metab. 2019;30(3):477–92 (e6).PubMedPubMedCentralCrossRef
104.
Certo M, et al. Endothelial cell and T-cell crosstalk: targeting metabolism as a therapeutic approach in chronic inflammation. Br J Pharmacol. 2021;178(10):2041–59.PubMedCrossRef
105.
106.
Perl A. mTOR activation is a biomarker and a central pathway to autoimmune disorders, cancer, obesity, and aging. Ann N Y Acad Sci. 2015;1346(1):33–44.PubMedPubMedCentralCrossRef
107.
Yang H, et al. MTORC1 coordinates the autophagy and apoptosis signaling in articular chondrocytes in osteoarthritic temporomandibular joint. Autophagy. 2020;16(2):271–88.PubMedCrossRef
108.
Nnah IC, et al. TFEB-driven endocytosis coordinates MTORC1 signaling and autophagy. Autophagy. 2019;15(1):151–64.PubMedCrossRef
109.
Reznick RM, et al. Aging-associated reductions in AMP-activated protein kinase activity and mitochondrial biogenesis. Cell Metab. 2007;5(2):151–6.PubMedPubMedCentralCrossRef
110.
111.
112.
Xiong Y, et al. hPMSCs-derived exosomal miRNA-21 protects against aging-related oxidative damage of CD4(+) T cells by targeting the PTEN/PI3K-Nrf2 axis. Front Immunol. 2021;12: 780897.PubMedPubMedCentralCrossRef
113.
114.
115.
Gamal RM, et al. Telomere dysfunction-related serological markers and oxidative stress markers in rheumatoid arthritis patients: correlation with diseases activity. Clin Rheumatol. 2018;37(12):3239–46.PubMedCrossRef
116.
Cao D, et al. Disruption of telomere Integrity and DNA repair machineries by KML001 induces T cell senescence, apoptosis, and cellular dysfunctions. Front Immunol. 2019;10:1152.PubMedPubMedCentralCrossRef
117.
118.
Wang Y, et al. Cytoplasmic DNA sensing by KU complex in aged CD4(+) T cell potentiates T cell activation and aging-related autoimmune inflammation. Immunity. 2021;54(4):632–47 (e9).PubMedCrossRef
119.
120.
Cai WW, et al. Metabolic reprogramming as a key regulator in the pathogenesis of rheumatoid arthritis. Inflamm Res. 2020;69(11):1087–101.PubMedCrossRef
121.
Franco F, et al. Metabolic and epigenetic regulation of T-cell exhaustion. Nat Metab. 2020;2(10):1001–12.PubMedCrossRef
122.
123.
124.
McGuire PJ. Mitochondrial dysfunction and the aging immune system. Biol (Basel). 2019;8(2):26.
125.
Pucino V, et al. Lactate buildup at the site of chronic inflammation promotes disease by inducing CD4(+) T cell metabolic rewiring. Cell Metab. 2019;30(6):1055–74 (e8).PubMedPubMedCentralCrossRef
126.
Yang Z, et al. Restoring oxidant signaling suppresses proarthritogenic T cell effector functions in rheumatoid arthritis. Sci Transl Med. 2016;8(331):331ra38.PubMedPubMedCentralCrossRef
127.
Davalli P, et al. ROS, cell senescence, and novel molecular mechanisms in aging and age-related diseases. Oxid Med Cell Longev. 2016;2016:3565127.PubMedPubMedCentralCrossRef
128.
Lavin MF, et al. ATM-dependent phosphorylation of all three members of the MRN complex: from sensor to adaptor. Biomolecules. 2015;5(4):2877–902.PubMedPubMedCentralCrossRef
129.
130.
Myers DR, Wheeler B, Roose JP. mTOR and other effector kinase signals that impact T cell function and activity. Immunol Rev. 2019;291(1):134–53.PubMedPubMedCentralCrossRef
131.
Lin SC, Hardie DG. AMPK: sensing glucose as well as cellular energy status. Cell Metab. 2018;27(2):299–313.PubMedCrossRef
132.
133.
134.
Kundu-Raychaudhuri S, Abria C, Raychaudhuri SP. IL-9, a local growth factor for synovial T cells in inflammatory arthritis. Cytokine. 2016;79:45–51.PubMedCrossRef
135.
136.
137.
138.
Callender LA, et al. Mitochondrial mass governs the extent of human T cell senescence. Aging Cell. 2020;19(2): e13067.PubMedCrossRef
139.
140.
141.
Jiang Y, et al. Caveolin-1 controls mitochondrial damage and ROS production by regulating fission-fusion dynamics and mitophagy. Redox Biol. 2022;52: 102304.PubMedPubMedCentralCrossRef
142.
143.
Fakouri NB, et al. Toward understanding genomic instability, mitochondrial dysfunction and aging. FEBS J. 2019;286(6):1058–73.PubMedCrossRef
144.
Raz Y, et al. Activation-induced autophagy Is preserved in CD4+ T-cells in familial longevity. J Gerontol A Biol Sci Med Sci. 2017;72(9):1201–6.PubMedPubMedCentralCrossRef
145.
Bektas A, et al. Age-associated changes in human CD4(+) T cells point to mitochondrial dysfunction consequent to impaired autophagy. Aging (Albany NY). 2019;11(21):9234–63.CrossRef
146.
Vaena S, et al. Aging-dependent mitochondrial dysfunction mediated by ceramide signaling inhibits antitumor T cell response. Cell Rep. 2021;35(5): 109076.PubMedPubMedCentralCrossRef
147.
Wyman B, Perl A. Metabolic pathways mediate pathogenesis and offer targets for treatment in rheumatic diseases. Curr Opin Rheumatol. 2020;32(2):184–91.PubMedPubMedCentralCrossRef
148.
Tan S, et al. Platelet factor 4 enhances CD4(+) T effector memory cell responses via Akt-PGC1alpha-TFAM signaling-mediated mitochondrial biogenesis. J Thromb Haemost. 2020;18(10):2685–700.PubMedCrossRef
149.
150.
Willinger T, Flavell RA. Canonical autophagy dependent on the class III phosphoinositide-3 kinase Vps34 is required for naive T-cell homeostasis. Proc Natl Acad Sci USA. 2012;109(22):8670–5.PubMedPubMedCentralCrossRef
151.
152.
Wu D, Prives C. Relevance of the p53-MDM2 axis to aging. Cell Death Differ. 2018;25(1):169–79.PubMedCrossRef
153.
Blandino G, et al. Wild type- and mutant p53 proteins in mitochondrial dysfunction: emerging insights in cancer disease. Semin Cell Dev Biol. 2020;98:105–17.PubMedCrossRef
154.
Liu B, Li J, Cairns MJ. Identifying miRNAs, targets and functions. Brief Bioinform. 2014;15(1):1–19.PubMedCrossRef
155.
Kabekkodu SP, et al. Clustered miRNAs and their role in biological functions and diseases. Biol Rev Camb Philos Soc. 2018;93(4):1955–86.PubMedCrossRef
156.
Lu Q, et al. miRNAs as therapeutic targets in inflammatory disease. Trends Pharmacol Sci. 2019;40(11):853–65.PubMedCrossRef
157.
Kroesen BJ, et al. Immuno-miRs: critical regulators of T-cell development, function and ageing. Immunology. 2015;144(1):1–10.PubMedCrossRef
158.
159.
Gustafson CE, et al. Functional pathways regulated by microRNA networks in CD8 T-cell aging. Aging Cell. 2019;18(1): e12879.PubMedCrossRef
160.
161.
162.
Yang P, et al. MicroRNA let-7g-5p alleviates murine collagen-induced arthritis by inhibiting Th17 cell differentiation. Biochem Pharmacol. 2020;174: 113822.PubMedCrossRef
163.
Jin S, et al. Protectin DX restores Treg/Th17 cell balance in rheumatoid arthritis by inhibiting NLRP3 inflammasome via miR-20a. Cell Death Dis. 2021;12(3):280.PubMedPubMedCentralCrossRef
164.
Cheng NL, et al. MicroRNA-125b modulates inflammatory chemokine CCL4 expression in immune cells and its reduction causes CCL4 increase with age. Aging Cell. 2015;14(2):200–8.PubMedPubMedCentralCrossRef
165.
Evangelatos G, et al. MicroRNAs in rheumatoid arthritis: from pathogenesis to clinical impact. Autoimmun Rev. 2019;18(11): 102391.PubMedCrossRef
166.
167.
Guo D, et al. Study of miRNA interactome in active rheumatoid arthritis patients reveals key pathogenic roles of dysbiosis in the infection-immune network. Rheumatol (Oxford). 2021;60(3):1512–22.CrossRef
168.
Hanlon P, et al. Frailty in rheumatoidrmdopen arthritis and its relationship with disease activity, hospitalisation and mortality: a longitudinal analysis of the scottish early rheumatoid arthritis cohort and UK Biobank. RMD Open. 2022;8(1):e002111.PubMedPubMedCentralCrossRef
169.
Salaffi F et al. Inflammaging and frailty in immune-mediated rheumatic diseases: how to address and score the issue. Clin Rev Allergy Immunol. 2022;8(1):e002111.
Metadaten
Titel
Immunosenescence of T cells: a key player in rheumatoid arthritis
verfasst von
Yi Gao
Weiwei Cai
Ying Zhou
Yuhui Li
Jingwen Cheng
Fang Wei
Publikationsdatum
25.10.2022
Verlag
Springer International Publishing
Erschienen in
Inflammation Research / Ausgabe 12/2022
Print ISSN: 1023-3830
Elektronische ISSN: 1420-908X
DOI
https://doi.org/10.1007/s00011-022-01649-0

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