Login Register Cart 0
Generic placeholder image

Current Stem Cell Research & Therapy

Editor-in-Chief

ISSN (Print): 1574-888X
ISSN (Online): 2212-3946

Back
Journal Home About Journal Editorial Board Journal Insight Current Issue Volumes/Issues
Subscribe
Review Article

Differentiation of Pancreatic Beta Cells: Dual Acting of Inflammatory Factors

Author(s): Faeze Shahedi, Arron Munggela Foma, Azam Mahmoudi-Aznaveh, Mohammad Ali Mazlomi, Zahra Azizi* and Mohammad Reza Khorramizadeh*

Volume 19, Issue 6, 2024

Published on: 06 July, 2023

Page: [832 - 839] Pages: 8

DOI: 10.2174/1574888X18666230504093649

Price: $65

Abstract

In the past decades, scientists have made outstanding efforts to treat diabetes. However, diabetes treatment is still far from satisfactory due to the complex nature of the disease and the challenges encountered in resolving it. Inflammatory factors are key regulators of the immune system's response to pathological insults, organ neogenesis, rejuvenation of novel cells to replace injured cells and overwhelming disease conditions. Currently, the available treatments for type 1 diabetes include daily insulin injection, pancreatic beta cell or tissue transplantation, and gene therapy. Cell therapy, exploiting differentiation, and reprogramming various types of cells to generate pancreatic insulin-producing cells are novel approaches for the treatment of type 1 diabetes. A better understanding of the inflammatory pathways offers valuable and improved therapeutic options to provide more advanced and better treatments for diabetes. In this review, we investigated different types of inflammatory factors that participate in the pathogenesis of type 1 diabetes, their possible dual impacts on the differentiation, reprogramming, and fusion of other stem cell lines into pancreatic insulin-producing beta cells, and the possibility of applying these factors to improve the treatment of this disease.

Keywords: Autoimmunity, leukocytes, pathogens, pancreatic beta cell, type 1 diabetes, cytokines.

« Previous Next »
Graphical Abstract

[1]
Rotondi M, Chiovato L, Romagnani S, Serio M, Romagnani P. Role of chemokines in endocrine autoimmune diseases. Endocr Rev 2007; 28(5): 492-520.
[http://dx.doi.org/10.1210/er.2006-0044] [PMID: 17475924]
[2]
Turley S, Poirot L, Hattori M, Benoist C, Mathis D. Physiological beta cell death triggers priming of self-reactive T cells by dendritic cells in a type-1 diabetes model. J Exp Med 2003; 198(10): 1527-37.
[http://dx.doi.org/10.1084/jem.20030966] [PMID: 14623908]
[3]
Tanaka S, Nishida Y, Aida K, et al. Enterovirus infection, CXC chemokine ligand 10 (CXCL10), and CXCR3 circuit: A mechanism of accelerated beta-cell failure in fulminant type 1 diabetes. Diabetes 2009; 58(10): 2285-91.
[http://dx.doi.org/10.2337/db09-0091] [PMID: 19641142]
[4]
Sarkar SA, Lee CE, Victorino F, et al. Expression and regulation of chemokines in murine and human type 1 diabetes. Diabetes 2012; 61(2): 436-46.
[http://dx.doi.org/10.2337/db11-0853] [PMID: 22210319]
[5]
Ardestani A, Maedler K. The hippo signaling pathway in pancreatic β-cells: Functions and regulations. Endocr Rev 2018; 39(1): 21-35.
[http://dx.doi.org/10.1210/er.2017-00167] [PMID: 29053790]
[6]
Geravandi S, Mahmoudi-aznaveh A, Azizi Z, Maedler K, Ardestani A. SARS-CoV-2 and pancreas: A potential pathological interaction? Trends Endocrinol Metab 2021; 32(11): 842-5.
[http://dx.doi.org/10.1016/j.tem.2021.07.004] [PMID: 34373155]
[7]
Gagnerault MC, Luan JJ, Lotton C, Lepault F. Pancreatic lymph nodes are required for priming of beta cell reactive T cells in NOD mice. J Exp Med 2002; 196(3): 369-77.
[http://dx.doi.org/10.1084/jem.20011353] [PMID: 12163565]
[8]
Spears E, Serafimidis I, Powers AC, Gavalas A. Debates in pancreatic beta cell biology: Proliferation versus progenitor differentiation and transdifferentiation in restoring β cell mass. Front Endocrinol 2021; 12: 722250.
[http://dx.doi.org/10.3389/fendo.2021.722250] [PMID: 34421829]
[9]
Rhode A, Pauza ME, Barral AM, Rodrigo E, Oldstone MB, von Herrath MG, et al. Islet-specific expression of CXCL10 causes spontaneous islet infiltration and accelerates diabetes development. J Immunol 2005; 175(6): 3516-24.
[http://dx.doi.org/10.4049/jimmunol.175.6.3516]
[10]
Mallone R, Brezar V, Boitard C. T cell recognition of autoantigens in human type 1 diabetes: clinical perspectives. Clin Dev Immunol 2011; 2011: 513210.
[http://dx.doi.org/10.1155/2011/513210] [PMID: 21785617]
[11]
Roep BO, Kracht MJL, van Lummel M, Zaldumbide A. A roadmap of the generation of neoantigens as targets of the immune system in type 1 diabetes. Curr Opin Immunol 2016; 43: 67-73.
[http://dx.doi.org/10.1016/j.coi.2016.09.007] [PMID: 27723537]
[12]
McLaughlin RJ, de Haan A, Zaldumbide A, et al. Human islets and dendritic cells generate post-translationally modified islet autoantigens. Clin Exp Immunol 2016; 185(2): 133-40.
[http://dx.doi.org/10.1111/cei.12775] [PMID: 26861694]
[13]
Eizirik DL, Sammeth M, Bouckenooghe T, et al. The human pancreatic islet transcriptome: Expression of candidate genes for type 1 diabetes and the impact of pro-inflammatory cytokines. PLoS Genet 2012; 8(3): e1002552.
[http://dx.doi.org/10.1371/journal.pgen.1002552] [PMID: 22412385]
[14]
Costes S, Bertrand G, Ravier MA. Mechanisms of beta-cell apoptosis in type 2 diabetes-prone situations and potential protection by GLP-1-based therapies. Int J Mol Sci 2021; 22(10): 5303.
[http://dx.doi.org/10.3390/ijms22105303] [PMID: 34069914]
[15]
Knip M, Siljander H. The role of the intestinal microbiota in type 1 diabetes mellitus. Nat Rev Endocrinol 2016; 12(3): 154-67.
[http://dx.doi.org/10.1038/nrendo.2015.218] [PMID: 26729037]
[16]
Kostic AD, Gevers D, Siljander H, et al. The dynamics of the human infant gut microbiome in development and in progression toward type 1 diabetes. Cell Host Microbe 2015; 17(2): 260-73.
[http://dx.doi.org/10.1016/j.chom.2015.01.001] [PMID: 25662751]
[17]
Zhang X, Zhivaki D, Lo-Man R. Unique aspects of the perinatal immune system. Nat Rev Immunol 2017; 17(8): 495-507.
[http://dx.doi.org/10.1038/nri.2017.54] [PMID: 28627520]
[18]
Kawabe T, Jankovic D, Kawabe S, et al. Memory-phenotype CD4 + T cells spontaneously generated under steady-state conditions exert innate TH 1-like effector function. Sci Immunol 2017; 2(12): eaam9304.
[http://dx.doi.org/10.1126/sciimmunol.aam9304] [PMID: 28783663]
[19]
Kieper WC, Troy A, Burghardt JT, Ramsey C, Lee JY, Jiang HQ, et al. Recent immune status determines the source of antigens that drive homeostatic T cell expansion. Journal of immunology 2005; 174(6): 3158-63.
[http://dx.doi.org/10.4049/jimmunol.174.6.3158]
[20]
Jameson SC, Lee YJ, Hogquist KA. Innate memory T cells. Adv Immunol 2015; 126: 173-213.
[http://dx.doi.org/10.1016/bs.ai.2014.12.001] [PMID: 25727290]
[21]
Christianson SW, Shultz LD, Leiter EH. Adoptive transfer of diabetes into immunodeficient NOD-scid/scid mice. Relative contributions of CD4+ and CD8+ T-cells from diabetic versus prediabetic NOD.NON-Thy-1a donors. Diabetes 1993; 42(1): 44-55.
[http://dx.doi.org/10.2337/diab.42.1.44] [PMID: 8093606]
[22]
Wen L, Ley RE, Volchkov PY, et al. Innate immunity and intestinal microbiota in the development of Type 1 diabetes. Nature 2008; 455(7216): 1109-13.
[http://dx.doi.org/10.1038/nature07336] [PMID: 18806780]
[23]
Yang W, Cong Y. Gut microbiota-derived metabolites in the regulation of host immune responses and immune-related inflammatory diseases. Cell Mol Immunol 2021; 18(4): 866-77.
[http://dx.doi.org/10.1038/s41423-021-00661-4] [PMID: 33707689]
[24]
Wu W, Syed F, Simpson E, et al. Impact of proinflammatory cytokines on alternative splicing patterns in human islets. Diabetes 2022; 71(1): 116-27.
[http://dx.doi.org/10.2337/db20-0847]
[25]
Pan G, Mu Y, Hou L, Liu J. Examining the therapeutic potential of various stem cell sources for differentiation into insulin-producing cells to treat diabetes. Ann Endocrinol 2019; 80(1): 47-53.
[http://dx.doi.org/10.1016/j.ando.2018.06.1084] [PMID: 30041820]
[26]
Azizi Z, Lange C, Paroni F, et al. β-MSCs: Successful fusion of MSCs with β-cells results in a β-cell like phenotype. Oncotarget 2016; 7(31): 48963-77.
[http://dx.doi.org/10.18632/oncotarget.10214] [PMID: 27374092]
[27]
Amer MG, Embaby AS, Karam RA, Amer MG. Role of adipose tissue derived stem cells differentiated into insulin producing cells in the treatment of type I diabetes mellitus. Gene 2018; 654: 87-94.
[http://dx.doi.org/10.1016/j.gene.2018.02.008] [PMID: 29452233]
[28]
Chen YJ, Finkbeiner SR, Weinblatt D, et al. De novo formation of insulin-producing “neo-β cell islets” from intestinal crypts. Cell Rep 2014; 6(6): 1046-58.
[http://dx.doi.org/10.1016/j.celrep.2014.02.013] [PMID: 24613355]
[29]
Boumaza I, Srinivasan S, Witt WT, et al. Autologous bone marrow-derived rat mesenchymal stem cells promote PDX-1 and insulin expression in the islets, alter T cell cytokine pattern and preserve regulatory T cells in the periphery and induce sustained normoglycemia. J Autoimmun 2009; 32(1): 33-42.
[http://dx.doi.org/10.1016/j.jaut.2008.10.004] [PMID: 19062254]
[30]
Gao X, Song L, Shen K, et al. Bone marrow mesenchymal stem cells promote the repair of islets from diabetic mice through paracrine actions. Mol Cell Endocrinol 2014; 388(1-2): 41-50.
[http://dx.doi.org/10.1016/j.mce.2014.03.004] [PMID: 24667703]
[31]
Chen LB, Jiang XB, Yang L. Differentiation of rat marrow mesenchymal stem cells into pancreatic islet beta-cells. World J Gastroenterol 2004; 10(20): 3016-20.
[http://dx.doi.org/10.3748/wjg.v10.i20.3016] [PMID: 15378785]
[32]
Guan R, Purohit S, Wang H, et al. Chemokine (C-C motif) ligand 2 (CCL2) in sera of patients with type 1 diabetes and diabetic complications. PLoS One 2011; 6(4): e17822.
[http://dx.doi.org/10.1371/journal.pone.0017822] [PMID: 21532752]
[33]
Petropavlovskaia M, Makhlin J, Sampalis J, Rosenberg L. Development of an in vitro pancreatic tissue model to study regulation of islet neogenesis associated protein expression. J Endocrinol 2006; 191(1): 65-81.
[http://dx.doi.org/10.1677/joe.1.06800] [PMID: 17065390]
[34]
Tran DT, Pottekat A, Lee K, et al. Inflammatory cytokines rewire the proinsulin interaction network in human islets. J Clin Endocrinol Metab 2022; 107(11): 3100-10.
[http://dx.doi.org/10.1210/clinem/dgac493] [PMID: 36017587]
[35]
Hundhausen C, Roth A, Whalen E, Chen J, Schneider A, Long AS, et al. Enhanced T cell responses to IL-6 in type 1 diabetes are associated with early clinical disease and increased IL-6 receptor expression. Sci Transl Med 2017; 48(356): 995-1002.
[PMID: 27629486]
[36]
Kuriya G, Uchida T, Akazawa S, et al. Double deficiency in IL-17 and IFN-γ signalling significantly suppresses the development of diabetes in the NOD mouse. Diabetologia 2013; 56(8): 1773-80.
[http://dx.doi.org/10.1007/s00125-013-2935-8] [PMID: 23699989]
[37]
Ferreira RC, Simons HZ, Thompson WS, et al. IL-21 production by CD4+ effector T cells and frequency of circulating follicular helper T cells are increased in type 1 diabetes patients. Diabetologia 2015; 58(4): 781-90.
[http://dx.doi.org/10.1007/s00125-015-3509-8] [PMID: 25652388]
[38]
Sutherland APR, Van Belle T, Wurster AL, et al. Interleukin-21 is required for the development of type 1 diabetes in NOD mice. Diabetes 2009; 58(5): 1144-55.
[http://dx.doi.org/10.2337/db08-0882] [PMID: 19208913]
[39]
Wan XX, Zhang DY, Khan MA, et al. Stem cell transplantation in the treatment of type 1 Diabetes Mellitus: From insulin replacement to beta-cell replacement. Front Endocrinol 2022; 13: 859638.
[http://dx.doi.org/10.3389/fendo.2022.859638] [PMID: 35370989]
[40]
Silva IBB, Kimura CH, Colantoni VP, Sogayar MC. Stem cells differentiation into insulin-producing cells (IPCs): Recent advances and current challenges. Stem Cell Res Ther 2022; 13(1): 309.
[http://dx.doi.org/10.1186/s13287-022-02977-y] [PMID: 35840987]
[41]
Azizi Z, Abbaszadeh R, Sahebnasagh R, Norouzy A, Motevaseli E, Maedler K. Bone marrow mesenchymal stromal cells for diabetes therapy: Touch, fuse, and fix? Stem Cell Res Ther 2022; 13(1): 348.
[http://dx.doi.org/10.1186/s13287-022-03028-2] [PMID: 35883121]
[42]
Bourgeois S, Sawatani T, Van Mulders A, et al. Towards a functional cure for diabetes using stem cell-derived beta cells: Are we there yet? Cells 2021; 10(1): 191.
[http://dx.doi.org/10.3390/cells10010191] [PMID: 33477961]
[43]
de Klerk E, Hebrok M. Stem cell-based clinical trials for diabetes mellitus. Front Endocrinol 2021; 12: 631463.
[http://dx.doi.org/10.3389/fendo.2021.631463] [PMID: 33716982]
[44]
Ryba-Stanisławowska M, Rybarczyk-Kapturska K, Myśliwiec M, Myśliwska J. Elevated levels of serum IL-12 and IL-18 are associated with lower frequencies of CD4(+)CD25 (high)FOXP3 (+) regulatory Tcells in young patients with type 1 diabetes. Inflammation 2014; 37(5): 1513-20.
[http://dx.doi.org/10.1007/s10753-014-9878-1] [PMID: 24677179]
[45]
Homann D. Back from the brink: The uses of targeting the CXCL10:CXCR3 axis in Type 1 Diabetes. Diabetes 2015; 64(12): 3990-2.
[http://dx.doi.org/10.2337/dbi15-0019] [PMID: 26604174]

Rights & Permissions Print Cite
Article Metrics
16
2
© 2024 Bentham Science Publishers | Privacy Policy