Immune Response and Antigen-Specific Personalized Therapeutics in Multiple Sclerosis-the Upcoming Era of Precision Medicine

Dear Colleagues,

Multiple sclerosis (MS) is an autoimmune disorder characterized by T cell-mediated demyelination and neurodegeneration of the central nervous system (CNS) , whose exact etiology remains unclear. The autoimmune view of MS is strongly supported by the use of the animal experimental autoimmune encephalomyelitis (EAE) model, which displays some of the key MS characteristics. For example, during the activation phase, the antigen presenting cells (APCs) migrate to the lymph nodes and present the immunodominant peptide to naïve T cells, and the histocompatibility (MHC) Class II-restricted CD4+ T cells secrete many inflammatory cytokines such as IFN-y, TNFα, IL-6, and IL-17. During the effector phase, CD4+ T cells that recognize antigen proliferate, cross the blood–brain barrier (BBB) and subsequently activate macrophages and microglia that cause demyelination, oligodendrocyte death, and axon degeneration. As the disease progresses, remyelination and regeneration of oligodendrocyte become inefficient and ultimately fail, resulting in disease progression.

B cells were recently identified as core APCs to T cells, among other functions, involved strongly with immune response in MS pathophysiology, while many B-targeted therapies were introduced and established in MS therapeutics. Bruton tyrosine kinase (BTK) plays an indispensable role in B cells in signaling from the B cell receptor (BCR) for antigen. Thus, recently, various BTK inhibitors (BTKi) are being studied in MS therapeutics, in phase III clinical trials.

Several MS treatment drugs have been effective in reducing immune responses, but their impact on long-term disease progression, accrual of irreversible neurological disability, and the function of the immune system remains largely unclear. The limitation of pharmacological immune-modulating treatments is due to both the relatively non-specific inhibition of immune responses leading to immunosuppression and the failure to repair the damaged myelin in the affected tissues.

Certain genetic, immunogenetic (HLA and non-HLA genes), epigenetic , multi-omic, immunological and gut–brain axis factors play a greater or lesser role in immune response and affect the response to existed immunotherapies in MS.                              

We are only beginning to understand the relationship between various factors to immune response and stratification of patients to responders and non-responders, regarding their response to various immunotherapies. However, our future aim as the neurological community is to select specific patients with MS as candidates for specific immunotherapies, especially personalized vaccination (antigen-specific) agents.

This Special Issue aims at gathering articles on immune response toward personalized therapeutics in MS, through the contribution of MS specialists around the world, taking into account the progress in the field in the last two decades.

Prof. Maria Anagnostouli
Prof. George P. Chrousos
Guest Editors

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• multiple sclerosis
• immune response
• immunopathogenesis
• T cells
• B cells
• antigen-presenting cells
• microglia
• antigens
• antibodies
• cytokines
• blood–brain barrier
• genetics
• immunogenetics
• immunotherapies
• vaccines
• personalized therapeutics
• precision medicine