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Derakhshani A, Asadzadeh Z, Safarpour H, et al. Regulation of CTLA-4 and PD-L1 Expression in Relapsing-Remitting Multiple Sclerosis Patients after Treatment with Fingolimod, IFNβ-1α, Glatiramer Acetate, and Dimethyl Fumarate Drugs. J Pers Med. 2021;11(8)doi: 10.3390/jpm11080721.
Derakhshani, A., Asadzadeh, Z., Safarpour, H., Leone, P., Shadbad, M. A., Heydari, A., Baradaran, B., & Racanelli, V. (2021). Regulation of CTLA-4 and PD-L1 Expression in Relapsing-Remitting Multiple Sclerosis Patients after Treatment with Fingolimod, IFNβ-1α, Glatiramer Acetate, and Dimethyl Fumarate Drugs. Journal of personalized medicine, 11(8), . https://doi.org/10.3390/jpm11080721
Derakhshani, Afshin, et al. "Regulation of CTLA-4 and PD-L1 Expression in Relapsing-Remitting Multiple Sclerosis Patients after Treatment with Fingolimod, IFNβ-1α, Glatiramer Acetate, and Dimethyl Fumarate Drugs." Journal of personalized medicine vol. 11,8 (2021). doi: https://doi.org/10.3390/jpm11080721
Derakhshani A, Asadzadeh Z, Safarpour H, Leone P, Shadbad MA, Heydari A, Baradaran B, Racanelli V. Regulation of CTLA-4 and PD-L1 Expression in Relapsing-Remitting Multiple Sclerosis Patients after Treatment with Fingolimod, IFNβ-1α, Glatiramer Acetate, and Dimethyl Fumarate Drugs. J Pers Med. 2021 Jul 27;11(8). doi: 10.3390/jpm11080721. PMID: 34442365; PMCID: PMC8400811.
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J Pers Med. 2021 Jul 27;11(8). doi: 10.3390/jpm11080721.

Regulation of CTLA-4 and PD-L1 Expression in Relapsing-Remitting Multiple Sclerosis Patients after Treatment with Fingolimod, IFNβ-1α, Glatiramer Acetate, and Dimethyl Fumarate Drugs.

Journal of personalized medicine

Afshin Derakhshani, Zahra Asadzadeh, Hossein Safarpour, Patrizia Leone, Mahdi Abdoli Shadbad, Ali Heydari, Behzad Baradaran, Vito Racanelli

Affiliations

  1. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz 516615731, Iran.
  2. IRCCS Istituto Tumori "Giovanni Paolo II" of Bari, 70124 Bari, Italy.
  3. Cellular and Molecular Research Center, Birjand University of Medical Sciences, Birjand 9717853577, Iran.
  4. Department of Biomedical Sciences and Human Oncology, University of Bari "Aldo Moro", 70124 Bari, Italy.
  5. Student Research Committee, Tabriz University of Medical Sciences, Tabriz 516615731, Iran.
  6. Department of Applied Mathematics, University of California, Merced, CA 95343, USA.
  7. Health Sciences Research Institute, University of California, Merced, CA 95343, USA.
  8. Department of Immunology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz 516615731, Iran.

PMID: 34442365 PMCID: PMC8400811 DOI: 10.3390/jpm11080721

Abstract

Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system (CNS) that is characterized by inflammation which typically results in significant impairment in most patients. Immune checkpoints act as co-stimulatory and co-inhibitory molecules and play a fundamental role in keeping the equilibrium of the immune system. Cytotoxic T-lymphocyte antigen-4 (CTLA-4) and Programmed death-ligand 1 (PD-L1), as inhibitory immune checkpoints, participate in terminating the development of numerous autoimmune diseases, including MS. We assessed the CTLA-4 and PD-L1 gene expression in the different cell types of peripheral blood mononuclear cells of MS patients using single-cell RNA-seq data. Additionally, this study outlines how CTLA-4 and PD-L1 expression was altered in the PBMC samples of relapsing-remitting multiple sclerosis (RRMS) patients compared to the healthy group. Finally, it investigates the impact of various MS-related treatments in the CTLA-4 and PD-L1 expression to restrain autoreactive T cells and stop the development of MS autoimmunity.

Keywords: CTLA-4; MS; PBMC; PD-L1; single-cell RNA-seq

References

  1. Cell J. 2017 Apr-Jun;19(1):1-10 - PubMed
  2. Front Immunol. 2018 Oct 08;9:2306 - PubMed
  3. Gene. 2021 Feb 15;769:145236 - PubMed
  4. Int Immunopharmacol. 2020 Mar;80:106221 - PubMed
  5. J Autoimmun. 2019 Jan;96:40-49 - PubMed
  6. Trends Immunol. 2013 Nov;34(11):556-63 - PubMed
  7. Neurology. 2008 Sep 16;71(12):917-24 - PubMed
  8. Sci Rep. 2018 Jul 19;8(1):10910 - PubMed
  9. Nat Rev Clin Oncol. 2019 Sep;16(9):563-580 - PubMed
  10. Life Sci Alliance. 2020 Jun 9;3(7): - PubMed
  11. World J Exp Med. 2014 Aug 20;4(3):27-37 - PubMed
  12. Immunology. 2009 Sep;128(1 Suppl):e787-96 - PubMed
  13. Med (N Y). 2021 Mar 12;2(3):296-312.e8 - PubMed
  14. J Autoimmun. 2019 Nov;104:102333 - PubMed
  15. J Neuroimmunol. 2012 Jan 18;242(1-2):39-46 - PubMed
  16. Clin Exp Immunol. 2017 Oct;190(1):1-7 - PubMed
  17. Genome Biol. 2018 Feb 6;19(1):15 - PubMed
  18. Nat Rev Drug Discov. 2010 Nov;9(11):883-97 - PubMed
  19. Nat Methods. 2013 Nov;10(11):1093-5 - PubMed
  20. Ann Neurol. 2011 Feb;69(2):292-302 - PubMed
  21. Proc Natl Acad Sci U S A. 2016 Apr 26;113(17):E2383-92 - PubMed
  22. J Neuroimmunol. 2018 Oct 15;323:105-108 - PubMed
  23. Immunol Rev. 2012 Jul;248(1):122-39 - PubMed
  24. Cell Immunol. 2016 Dec;310:27-41 - PubMed
  25. Nat Commun. 2020 Jan 14;11(1):247 - PubMed
  26. Iran J Allergy Asthma Immunol. 2016 Aug;15(4):296-302 - PubMed
  27. Nat Biotechnol. 2018 Dec 03;: - PubMed
  28. Front Neurol. 2018 Jan 23;9:5 - PubMed
  29. J Immunol. 2009 Jan 1;182(1):274-82 - PubMed
  30. Trends Mol Med. 2010 Feb;16(2):58-68 - PubMed
  31. Neurol Neuroimmunol Neuroinflamm. 2015 Dec 10;3(1):e183 - PubMed
  32. P T. 2012 Mar;37(3):175-84 - PubMed
  33. Exp Mol Med. 2018 Aug 7;50(8):1-14 - PubMed
  34. J Exp Med. 2000 Aug 7;192(3):393-404 - PubMed
  35. Neurotherapeutics. 2007 Oct;4(4):647-53 - PubMed

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