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Targeting Chemokines and Chemokine Receptors in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis

Authors Dhaiban S, Al-Ani M, Elemam NM, Maghazachi AA

Received 14 July 2020

Accepted for publication 27 August 2020

Published 29 September 2020 Volume 2020:13 Pages 619—633


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Editor who approved publication: Dr Ning Quan

Sarah Dhaiban, Mena Al-Ani, Noha Mousaad Elemam, Azzam A Maghazachi

College of Medicine and Immuno-Oncology Group, Sharjah Institute for Medical Research, University of Sharjah, Sharjah, United Arab Emirates

Correspondence: Azzam A Maghazachi
Department of Clinical Sciences, College of Medicine, University of Sharjah, Sharjah 27272, United Arab Emirates

Abstract: Multiple sclerosis (MS) is an immune-mediated and neurodegenerative disorder that results in inflammation and demyelination of the central nervous system (CNS). MS symptoms include walking difficulties, visual weakening, as well as learning and memory impairment, thus affecting the quality of the patient’s life. Chemokines and chemokine receptors are expressed on the immune cells as well as the CNS resident cells. Several sets of chemokine receptors and their ligands tend to be pathogenic players in MS, including CCL2, CCL3, CCL4, CCL5, CCL7, CCL8, CCL11, CCL17, CCL19, CCL21, CCL22, CXCL1, CXCL8, CXCL9, CXCL10, CXCL11, and CXCL16. Furthermore, current modulatory drugs that are used in the treatment of MS and its animal model, the experimental autoimmune encephalomyelitis (EAE), affect the expression of several chemokine and chemokine receptors. In this review, we highlight the pathogenic roles of chemokines and their receptors as well as utilizing them as potential therapeutic targets through selective agents, such as specific antibodies and receptor blockers, or indirectly through MS or EAE immunomodulatory drugs.

Keywords: multiple sclerosis, experimental autoimmune encephalomyelitis, chemokines, chemokine receptors

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