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Article

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

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
*
Authors to whom correspondence should be addressed.
These authors contributed equally to this work.
J. Pers. Med. 2021, 11(8), 721; https://doi.org/10.3390/jpm11080721
Submission received: 4 June 2021 / Revised: 29 June 2021 / Accepted: 20 July 2021 / Published: 27 July 2021
(This article belongs to the Special Issue Personalized Medicine for Multiple Sclerosis)

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

Share and Cite

MDPI and ACS Style

Derakhshani, A.; Asadzadeh, Z.; Safarpour, H.; Leone, P.; Shadbad, M.A.; 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, 11, 721. https://doi.org/10.3390/jpm11080721

AMA Style

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. Journal of Personalized Medicine. 2021; 11(8):721. https://doi.org/10.3390/jpm11080721

Chicago/Turabian Style

Derakhshani, Afshin, Zahra Asadzadeh, Hossein Safarpour, Patrizia Leone, Mahdi Abdoli Shadbad, Ali Heydari, Behzad Baradaran, and Vito Racanelli. 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, no. 8: 721. https://doi.org/10.3390/jpm11080721

APA Style

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), 721. https://doi.org/10.3390/jpm11080721

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