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Current Respiratory Medicine Reviews

Editor-in-Chief

ISSN (Print): 1573-398X
ISSN (Online): 1875-6387

Mini-Review Article

Evaluation of DPP4/CD26 Potential Role for the Management of Inflammation in COVID-19 Patients

Author(s): Fatemeh Akbarian*, Sanam Rezazadeh Chafjiri, Marziye Poornabi, Farzaneh Khani, Solmaz Abolhasanzadeh and Fatemeh Sadat Hosseini

Volume 19, Issue 3, 2023

Published on: 18 August, 2023

Page: [180 - 189] Pages: 10

DOI: 10.2174/1573398X19666230724155039

Price: $65

Open Access Journals Promotions 2
Abstract

Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for Coronavirus Disease 2019 (COVID-19) pandemic. Cell entry of the virus can be mediated by several enzymes, such as ACE-2, DPP4/CD26, and TMPRSS2, upon viral membrane fusion through SARS-CoV-2 envelope spike glycoproteins. In docked molecular complexes, DPP4/CD26 functional receptors and viral spike proteins have a large interface, potentially leading to inflammation in severe COVID-19.

Objective: The aim of this study is to review the role of DPP4/CD26 in the immune system and its effects on the production of cytokine storms in COVID-19. Furthermore, we hypothesize that targeting DPP4/CD26 as a therapeutic strategy could reduce the inflammatory complications of SARS-CoV-2 infection.

Methods: The current review was conducted using keywords such as COVID-19, SARS-CoV-2, dipeptidyl peptidase-4, CD26, cytokine storm, and treatment to search for articles in Google Scholar and PubMed databases that were specifically oriented towards our objectives.

Results: The regulation or inhibition of DPP4/CD26 might affect one or more stages in COVID-19 immuno- pathogenesis due to its associations with many immunological functions, such as modulating the NF-kB pathway, upregulating CD86 expression, activating proliferation of T cells, and influencing the antiviral response and cytokine storm in COVID-19. In this regard, the applications of DPP4/CD26 inhibitors, DPP4/CD26 siRNAs, and CD26 antibodies have been demonstrated to prevent cytokine storms and airway inflammation.

Conclusion: It is suggested to utilize novel technologies such as CRISPR/Cas and chimeric antigen receptor T cells, based on their many advantages, to increase the sensitivity and specificity of future treatment methods.

Keywords: COVID-19, SARS-CoV-2, dipeptidyl peptidase-4, CD26, T cell, cytokine storm.

Graphical Abstract
[1]
Naming the coronavirus disease (COVID-19) and the virus that causes it. Available at: https://www.who.int/emergencies/diseases/novel-coronavirus-2019/technical-guidance/naming-the-coronavirus-disease-(covid-2019)-and-the-virus-that-causes-it (accessed. on 2019).
[2]
Gorbalenya AE, Baker SC, Baric R, et al. Severe acute respiratory syndrome-related coronavirus: the species and its viruses-a statement of the coronavirus study group. biorxiv 2020.
[http://dx.doi.org/10.1101/2020.02.07.937862]
[3]
Notice on printing and distributing the pneumonia diagnosis and treatment plan for novel coronavirus infection Available at: http://www.gov.cn/zhengce/zhengceku/2020-02/05/content_5474791.htm (accessed on 2020).
[4]
Huang C, Wang Y, Li X, et al. Clinical features of patients infected with 2019 novel coronavirus in wuhan, china. Lancet 2022; 395(10223): 497-506.
[http://dx.doi.org/10.1016/S0140-6736(20)30183-5] [PMID: 31986264]
[5]
Zhu N, Zhang D, Wang W, et al. A novel coronavirus from patients with pneumonia in china, 2019. N Engl J Med 2020; 382(8): 727-33.
[http://dx.doi.org/10.1056/NEJMoa2001017] [PMID: 31978945]
[6]
Holshue ML, DeBolt C, Lindquist S, et al. First case of 2019 novel coronavirus in the united states. N Engl J Med 2020; 382(10): 929-36.
[http://dx.doi.org/10.1056/NEJMoa2001191] [PMID: 32004427]
[7]
Jiang Y, Rubin L, Peng T, et al. Cytokine storm in COVID-19: From viral infection to immune responses, diagnosis and therapy. Int J Biol Sci 2022; 18(2): 459-72.
[http://dx.doi.org/10.7150/ijbs.59272] [PMID: 35002503]
[8]
Sebastián-Martín A, Sánchez BG, Mora-Rodríguez JM, Bort A, Díaz-Laviada I. Role of dipeptidyl peptidase-4 (dpp4) on covid-19 physiopathology. Biomedicines 2022; 10(8): 2026.
[http://dx.doi.org/10.3390/biomedicines10082026] [PMID: 36009573]
[9]
Solerte SB, Di Sabatino A, Galli M, Fiorina P. Dipeptidyl peptidase-4 (dpp4) inhibition in covid-19. Acta Diabetol 2020; 57(7): 779-83.
[http://dx.doi.org/10.1007/s00592-020-01539-z] [PMID: 32506195]
[10]
Giugliano D, Sportiello L, Capuano A, Maiorino M, Rossi F, Esposito K. Dipeptidyl peptidase-4 inhibitors in type 2 diabetes therapy - focus on alogliptin. Drug Des Devel Ther 2013; 7: 989-1001.
[http://dx.doi.org/10.2147/DDDT.S37647] [PMID: 24068868]
[11]
Zhang T, Tong X, Zhang S, et al. The roles of dipeptidyl peptidase 4 (dpp4) and dpp4 inhibitors in different lung diseases: new evidence. Front Pharmacol 2021; 12: 731453.
[http://dx.doi.org/10.3389/fphar.2021.731453] [PMID: 34955820]
[12]
Dalan R, Bornstein SR, El-Armouche A, et al. The ace-2 in covid-19: foe or friend? Horm Metab Res 2020; 52(5): 257-63.
[http://dx.doi.org/10.1055/a-1155-0501] [PMID: 32340044]
[13]
Jia HP, Look DC, Shi L, et al. ACE2 receptor expression and severe acute respiratory syndrome coronavirus infection depend on differentiation of human airway epithelia. J Virol 2005; 79(23): 14614-21.
[http://dx.doi.org/10.1128/JVI.79.23.14614-14621.2005] [PMID: 16282461]
[14]
Kuba K, Imai Y, Rao S, et al. A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus-induced lung injury. Nat Med 2005; 11(8): 875-9.
[http://dx.doi.org/10.1038/nm1267] [PMID: 16007097]
[15]
Carlson J. Carlson, J. University of Minnesota to test three drugs for COVID-19 patients. Available at: https://www.startribune.com/university-of-minnesota-to-test-three-drugs-for-covid-patients/568766632/ (accessed on: 2020).
[16]
Casadevall A, Pirofski L. The convalescent sera option for containing COVID-19. J Clin Invest 2020; 130(4): 1545-8.
[http://dx.doi.org/10.1172/JCI138003] [PMID: 32167489]
[17]
Zhang H, Penninger JM, Li Y, Zhong N, Slutsky AS. Angiotensin-converting enzyme 2 (ACE2) as a SARS-CoV-2 receptor: Molecular mechanisms and potential therapeutic target. Intensive Care Med 2020; 46(4): 586-90.
[http://dx.doi.org/10.1007/s00134-020-05985-9] [PMID: 32125455]
[18]
Strollo R, Pozzilli P. DPP4 inhibition: preventing sars-cov -2 infection and/or progression of covid -19? Diabetes Metab Res Rev 2020; 36(8): e3330.
[http://dx.doi.org/10.1002/dmrr.3330] [PMID: 32336007]
[19]
Raj VS, Mou H, Smits SL, et al. Dipeptidyl peptidase 4 is a functional receptor for the emerging human coronavirus-EMC. Nature 2013; 495(7440): 251-4.
[http://dx.doi.org/10.1038/nature12005] [PMID: 23486063]
[20]
Vankadari N, Wilce JA. Emerging COVID-19 coronavirus: Glycan shield and structure prediction of spike glycoprotein and its interaction with human CD26. Emerg Microbes Infect 2020; 9(1): 601-4.
[http://dx.doi.org/10.1080/22221751.2020.1739565] [PMID: 32178593]
[21]
Kawasaki T, Chen W, Htwe YM, Tatsumi K, Dudek SM. DPP4 inhibition by sitagliptin attenuates LPS-induced lung injury in mice. Am J Physiol Lung Cell Mol Physiol 2018; 315(5): L834-45.
[http://dx.doi.org/10.1152/ajplung.00031.2018] [PMID: 30188745]
[22]
Klemann C, Wagner L, Stephan M, von Hörsten S. Cut to the chase: A review of CD26/dipeptidyl peptidase-4's (DPP4) entanglement in the immune system. Clin Exp Immunol 2016; 185(1): 1-21.
[http://dx.doi.org/10.1111/cei.12781] [PMID: 26919392]
[23]
Shao S, Xu Q, Yu X, Pan R, Chen Y. Dipeptidyl peptidase 4 inhibitors and their potential immune modulatory functions. Pharmacol Ther 2020; 209: 107503-3.
[http://dx.doi.org/10.1016/j.pharmthera.2020.107503] [PMID: 32061923]
[24]
Ohnuma K, Uchiyama M, Yamochi T, et al. Caveolin-1 triggers T-cell activation via CD26 in association with CARMA1. J Biol Chem 2007; 282(13): 10117-31.
[http://dx.doi.org/10.1074/jbc.M609157200] [PMID: 17287217]
[25]
Tisoncik JR, Korth MJ, Simmons CP, Farrar J, Martin TR, Katze MG. Into the eye of the cytokine storm. Microbiol Mol Biol Rev 2012; 76(1): 16-32.
[http://dx.doi.org/10.1128/MMBR.05015-11] [PMID: 22390970]
[26]
Rubenfeld GD, Caldwell E, Peabody E, et al. Incidence and outcomes of acute lung injury. N Engl J Med 2005; 353(16): 1685-93.
[http://dx.doi.org/10.1056/NEJMoa050333] [PMID: 16236739]
[27]
Xiong Y, Liu Y, Cao L, et al. Transcriptomic characteristics of bronchoalveolar lavage fluid and peripheral blood mononuclear cells in COVID-19 patients. Emerg Microbes Infect 2020; 9(1): 761-70.
[http://dx.doi.org/10.1080/22221751.2020.1747363] [PMID: 32228226]
[28]
Channappanavar R, Perlman S. Pathogenic human coronavirus infections: Causes and consequences of cytokine storm and immunopathology Seminars in immunopathology. Springer 2017; Vol. 39: pp. 529-39.
[http://dx.doi.org/10.1007/s00281-017-0629-x]
[29]
Fensterl V, Sen GC. Interferons and viral infections. Biofactors 2009; 35(1): 14-20.
[http://dx.doi.org/10.1002/biof.6] [PMID: 19319841]
[30]
Katze MG, Fornek JL, Palermo RE, Walters KA, Korth MJ. Innate immune modulation by RNA viruses: Emerging insights from functional genomics. Nat Rev Immunol 2008; 8(8): 644-54.
[http://dx.doi.org/10.1038/nri2377] [PMID: 18654572]
[31]
Friedman RM. Clinical uses of interferons. Br J Clin Pharmacol 2008; 65(2): 158-62.
[http://dx.doi.org/10.1111/j.1365-2125.2007.03055.x] [PMID: 18070219]
[32]
Borden EC, Sen GC, Uze G, et al. Interferons at age 50: Past, current and future impact on biomedicine. Nat Rev Drug Discov 2007; 6(12): 975-90.
[http://dx.doi.org/10.1038/nrd2422] [PMID: 18049472]
[33]
Brocker C, Thompson D, Matsumoto A, Nebert DW, Vasiliou V. Evolutionary divergence and functions of the human interleukin (IL) gene family. Hum Genomics 2010; 5(1): 30-55.
[http://dx.doi.org/10.1186/1479-7364-5-1-30] [PMID: 21106488]
[34]
Guarda G, Braun M, Staehli F, et al. Type I interferon inhibits interleukin-1 production and inflammasome activation. Immunity 2011; 34(2): 213-23.
[http://dx.doi.org/10.1016/j.immuni.2011.02.006] [PMID: 21349431]
[35]
Schmitz N, Kurrer M, Bachmann MF, Kopf M. Interleukin-1 is responsible for acute lung immunopathology but increases survival of respiratory influenza virus infection. J Virol 2005; 79(10): 6441-8.
[http://dx.doi.org/10.1128/JVI.79.10.6441-6448.2005] [PMID: 15858027]
[36]
Comerford I, McColl SR. Mini-review series: Focus on chemokines. Immunol Cell Biol 2011; 89(2): 183-4.
[http://dx.doi.org/10.1038/icb.2010.164] [PMID: 21326315]
[37]
Raman D, Sobolik-Delmaire T, Richmond A. Chemokines in health and disease. Exp Cell Res 2011; 317(5): 575-89.
[http://dx.doi.org/10.1016/j.yexcr.2011.01.005] [PMID: 21223965]
[38]
Garin A, Proudfoot AEI. Chemokines as targets for therapy. Exp Cell Res 2011; 317(5): 602-12.
[http://dx.doi.org/10.1016/j.yexcr.2010.12.021] [PMID: 21376173]
[39]
Hamilton JA. Colony-stimulating factors in inflammation and autoimmunity. Nat Rev Immunol 2008; 8(7): 533-44.
[http://dx.doi.org/10.1038/nri2356] [PMID: 18551128]
[40]
Beutler B, Milsark IW, Cerami AC. Passive immunization against cachectin/tumor necrosis factor protects mice from lethal effect of endotoxin. Science 1985; 229(4716): 869-71.
[http://dx.doi.org/10.1126/science.3895437] [PMID: 3895437]
[41]
Clark I. How TNF was recognized as a key mechanism of disease. Cytokine Growth Factor Rev 2007; 18(3-4): 335-43.
[http://dx.doi.org/10.1016/j.cytogfr.2007.04.002] [PMID: 17493863]
[42]
Clark IA, Virelizier JL, Carswell EA, Wood PR. Possible importance of macrophage-derived mediators in acute malaria. Infect Immun 1981; 32(3): 1058-66.
[http://dx.doi.org/10.1128/iai.32.3.1058-1066.1981] [PMID: 6166564]
[43]
Aggarwal BB. Signalling pathways of the TNF superfamily: A double-edged sword. Nat Rev Immunol 2003; 3(9): 745-56.
[http://dx.doi.org/10.1038/nri1184] [PMID: 12949498]
[44]
Park W, Goodman RB, Steinberg KP, et al. Cytokine balance in the lungs of patients with acute respiratory distress syndrome. Am J Respir Crit Care Med 2001; 164(10): 1896-903.
[http://dx.doi.org/10.1164/ajrccm.164.10.2104013] [PMID: 11734443]
[45]
Sun L, Louie MC, Vannella KM, et al. New concepts of IL-10-induced lung fibrosis: Fibrocyte recruitment and M 2 activation in a CCL2/CCR2 axis. Am J Physiol Lung Cell Mol Physiol 2011; 300(3): L341-53.
[http://dx.doi.org/10.1152/ajplung.00122.2010] [PMID: 21131395]
[46]
Rojas JM, Avia M, Martín V, Sevilla N. IL-10: A Multifunctional Cytokine in Viral Infections. J Immunol Res 2017; 2017: 1-14.
[http://dx.doi.org/10.1155/2017/6104054] [PMID: 28316998]
[47]
Roncati L, Lusenti B. The «moonlighting protein» able to explain the Th1 immune lockdown in severe COVID-19. Med Hypotheses 2020; 143: 110087.
[http://dx.doi.org/10.1016/j.mehy.2020.110087] [PMID: 32679426]
[48]
Tseng CTK, Perrone LA, Zhu H, Makino S, Peters CJ. Severe acute respiratory syndrome and the innate immune responses: Modulation of effector cell function without productive infection. J Immunol 2005; 174(12): 7977-85.
[http://dx.doi.org/10.4049/jimmunol.174.12.7977] [PMID: 15944304]
[49]
Xu Z, Shi L, Wang Y, et al. Pathological findings of COVID-19 associated with acute respiratory distress syndrome. Lancet Respir Med 2020; 8(4): 420-2.
[http://dx.doi.org/10.1016/S2213-2600(20)30076-X] [PMID: 32085846]
[50]
Reinhold D, Bank U, Bühling F, et al. Inhibitors of dipeptidyl peptidase IV (DP IV, CD26) induces secretion of transforming growth factor-β1 (TGF-β1) in stimulated mouse splenocytes and thymocytes. Immunol Lett 1997; 58(1): 29-35.
[http://dx.doi.org/10.1016/S0165-2478(97)02716-8] [PMID: 9436466]
[51]
Schön E, Demuth HU, Eichmann E, et al. Dipeptidyl peptidase IV in human T lymphocytes. Impaired induction of interleukin 2 and gamma interferon due to specific inhibition of dipeptidyl peptidase IV. Scand J Immunol 1989; 29(2): 127-32.
[http://dx.doi.org/10.1111/j.1365-3083.1989.tb01108.x] [PMID: 2564215]
[52]
Schade J, Stephan M, Schmiedl A, et al. Regulation of expression and function of dipeptidyl peptidase 4 (DP4), DP8/9, and DP10 in allergic responses of the lung in rats. J Histochem Cytochem 2008; 56(2): 147-55.
[http://dx.doi.org/10.1369/jhc.7A7319.2007] [PMID: 17967935]
[53]
Kruschinski C, Skripuletz T, Bedoui S, et al. CD26 (dipeptidyl-peptidase IV)-dependent recruitment of T cells in a rat asthma model. Clin Exp Immunol 2004; 139(1): 17-24.
[http://dx.doi.org/10.1111/j.1365-2249.2005.02666.x] [PMID: 15606609]
[54]
Radzikowska U, Ding M, Tan G, et al. Distribution of ACE2, CD147, CD26, and other SARS-CoV-2 associated molecules in tissues and immune cells in health and in asthma, COPD, obesity, hypertension, and COVID-19 risk factors. Allergy 2020; 75(11): 2829-45.
[http://dx.doi.org/10.1111/all.14429] [PMID: 32496587]
[55]
Yu DMT, Slaitini L, Gysbers V, et al. Soluble CD26/dipeptidyl peptidase IV enhances human lymphocyte proliferation in vitro independent of dipeptidyl peptidase enzyme activity and adenosine deaminase binding. Scand J Immunol 2011; 73(2): 102-11.
[http://dx.doi.org/10.1111/j.1365-3083.2010.02488.x] [PMID: 21198750]
[56]
Bassendine MF, Bridge SH, McCaughan GW, Gorrell MD. COVID-19 and comorbidities: A role for dipeptidyl peptidase 4 (DPP4) in disease severity? J Diabetes 2020; 12(9): 649-58.
[http://dx.doi.org/10.1111/1753-0407.13052] [PMID: 32394639]
[57]
Waumans Y, Baerts L, Kehoe K, Lambeir AM, De Meester I. The Dipeptidyl Peptidase Family, Prolyl Oligopeptidase, and Prolyl Carboxypeptidase in the Immune System and Inflammatory Disease, Including Atherosclerosis. Front Immunol 2015; 6: 387.
[http://dx.doi.org/10.3389/fimmu.2015.00387] [PMID: 26300881]
[58]
Ikeda T, Kumagai E, Iwata S, Yamakawa A. Soluble cd26/dipeptidyl peptidase iv enhances the transcription of il-6 and tnf-α in thp-1 cells and monocytes. PLoS One 2013; 8(6): e66520.
[http://dx.doi.org/10.1371/journal.pone.0066520] [PMID: 23805228]
[59]
Pedersen SF, Ho YC. SARS-CoV-2: A storm is raging. J Clin Invest 2020; 130(5): 2202-5.
[http://dx.doi.org/10.1172/JCI137647] [PMID: 32217834]
[60]
Al-Qahtani AA, Lyroni K, Aznaourova M, et al. Middle east respiratory syndrome corona virus spike glycoprotein suppresses macrophage responses via DPP4-mediated induction of IRAK-M and PPARγ. Oncotarget 2017; 8(6): 9053-66.
[http://dx.doi.org/10.18632/oncotarget.14754] [PMID: 28118607]
[61]
Lee YS, Park MS, Choung JS, et al. Glucagon-like peptide-1 inhibits adipose tissue macrophage infiltration and inflammation in an obese mouse model of diabetes. Diabetologia 2012; 55(9): 2456-68.
[http://dx.doi.org/10.1007/s00125-012-2592-3] [PMID: 22722451]
[62]
Lee YS, Jun HS. Anti-inflammatory effects of glp-1-based therapies beyond glucose control. Mediators Inflamm 2016; 2016: 1-11.
[http://dx.doi.org/10.1155/2016/3094642] [PMID: 27110066]
[63]
Morimoto C, Schlossman SF. The structure and function of CD26 in the T-cell immune response. Immunol Rev 1998; 161(1): 55-70.
[http://dx.doi.org/10.1111/j.1600-065X.1998.tb01571.x] [PMID: 9553764]
[64]
Dipeptidyl Peptidase-4 Inhibitor (DPP4i) for the Control of Hyperglycemia in Patients With COVID-19. Available at: https://clinicaltrials.gov/show/NCT04542213
[65]
Sitagliptin Treatment in Diabetic COVID-19 Positive Patients Available at: https://clinicaltrials.gov/show/NCT04382794
[66]
The Effect of Sitagliptin Treatment in COVID-19 Positive Diabetic Patients. Available at: https://clinicaltrials.gov/show/NCT04365517
[67]
Cockrell AS, Yount BL, Scobey T, et al. A mouse model for MERS coronavirus-induced acute respiratory distress syndrome. Nat Microbiol 2016; 2(2): 16226.
[http://dx.doi.org/10.1038/nmicrobiol.2016.226] [PMID: 27892925]
[68]
Bailey SR, Nelson MH, Majchrzak K, et al. Human CD26high T cells elicit tumor immunity against multiple malignancies via enhanced migration and persistence. Nat Commun 2017; 8(1): 1961.
[http://dx.doi.org/10.1038/s41467-017-01867-9] [PMID: 29213079]
[69]
Guo X, Kazanova A, Thurmond S, Saragovi HU, Rudd CE. Effective chimeric antigen receptor T cells against SARS-CoV-2. iScience 2021; 24(11): 103295.
[http://dx.doi.org/10.1016/j.isci.2021.103295] [PMID: 34693218]
[70]
Liu C, Zhou Q, Li Y, et al. Research and Development on Therapeutic Agents and Vaccines for COVID-19 and Related Human Coronavirus Diseases. ACS Cent Sci 2020; 6(3): 315-31.
[http://dx.doi.org/10.1021/acscentsci.0c00272] [PMID: 32226821]
[71]
Takahashi Y, Kawasaki T, Sato H, et al. Functional roles for cd26/dpp4 in mediating inflammatory responses of pulmonary vascular endothelial cells. Cells 2021; 10(12): 3508.
[http://dx.doi.org/10.3390/cells10123508] [PMID: 34944016]
[72]
Galimberti S, Morabito F, Gentile M, et al. Dipeptidyl-peptidase 4 (Cd26): a possible therapeutic target in Covid-19. Department of Clinical and Experimental Medicine 2020; 2(1)
[http://dx.doi.org/10.32474/LOJPCR.2020.02.000128]
[73]
Köhler G, Milstein C. Continuous cultures of fused cells secreting antibody of predefined specificity. Nature 1975; 256(5517): 495-7.
[http://dx.doi.org/10.1038/256495a0] [PMID: 1172191]
[74]
Palumbo A, Anderson K. Multiple Myeloma. N Engl J Med 2011; 364(11): 1046-60.
[http://dx.doi.org/10.1056/NEJMra1011442] [PMID: 21410373]
[75]
Ohnuma K, Haagmans BL, Hatano R, et al. Inhibition of Middle East respiratory syndrome coronavirus infection by anti-CD26 monoclonal antibody. J Virol 2013; 87(24): 13892-9.
[http://dx.doi.org/10.1128/JVI.02448-13] [PMID: 24067970]
[76]
Angevin E, Isambert N, Trillet-Lenoir V, et al. First-in-human phase 1 of ys110, a monoclonal antibody directed against cd26 in advanced cd26-expressing cancers. Br J Cancer 2017; 116(9): 1126-34.
[http://dx.doi.org/10.1038/bjc.2017.62] [PMID: 28291776]
[77]
Sorek R, Lawrence CM, Wiedenheft B. CRISPR-mediated adaptive immune systems in bacteria and archaea. Annu Rev Biochem 2013; 82(1): 237-66.
[http://dx.doi.org/10.1146/annurev-biochem-072911-172315] [PMID: 23495939]
[78]
Cho SW, Kim S, Kim J, Kim J-S. Targeted genome engineering in human cells with the Cas9 RNA-guided endonuclease. Nat Biotechnol 31: 230-232. Nat Biotechnol 2013; 31.
[http://dx.doi.org/10.1038/nbt.2507] [PMID: 23360966]
[79]
Redman M, King A, Watson C, King D. What is CRISPR/Cas9? Archives of disease in childhood - Education & practice edition 2016; 101(4): 213-5.
[http://dx.doi.org/10.1136/archdischild-2016-310459]
[80]
Schumann K, Lin S, Boyer E, et al. Generation of knock-in primary human T cells using Cas9 ribonucleoproteins. Proc Natl Acad Sci USA 2015; 112(33): 10437-42.
[http://dx.doi.org/10.1073/pnas.1512503112] [PMID: 26216948]
[81]
Cho EY, Ryu JY, Lee HAR, et al. Lecithin nano-liposomal particle as a CRISPR/Cas9 complex delivery system for treating type 2 diabetes. J Nanobiotechnology 2019; 17(1): 19.
[http://dx.doi.org/10.1186/s12951-019-0452-8] [PMID: 30696428]

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