The Immune System as a Target for Therapy of Progressive Multiple Sclerosis (MS) in Patients and Animal Models

Dear Colleagues,

The pathophysiology of Multiple Sclerosis (MS) is associated with an autoimmune chronic inflammation of the central nervous system (CNS), resulting in demyelination and neurodegeneration. The initial phase of the disease is presented by relapsing–remission, which, in most cases, is converted into secondary progressive MS (SPMS). A smaller number of patients (up to 15%) develop primary progressive MS (PPMS). In progressive MS (PMS), the relatively intact blood–brain barrier generates compartmentalized CNS immune inflammation, decorated by Ectopic Lymphoid Structures and characterized by accumulation of lymphocytes, macrophages and microglia. These cells release reactive oxygen and nitrogen species and pro-inflammatory cytokines/chemokines, leading to demyelination, axonal lesions and mitochondrial damage. While a relatively high number of disease-modifying therapies have shown efficacy in ameliorating relapsing–remitting MS (RRMS), the majority of these have been ineffective for PMS (e.g., copaxone, azathioprine) and the number of approved medications for PMS is very limited. The differential therapeutic effect between RRMS and PMS is possibly related to qualitative or quantitative differences in inflammatory phenotypes, e.g., distinct cell subpopulations, cytokines, profiles and inflammation sites. Analyzing these inflammatory phenotypes as well as other differences may help us to understand why beneficial medications are documented in RRMS, but not in PMS, what characteristics underline the few approved PMS medications, and how PMS drugs should be designed. The articles collected in this Special Issue of IJMS may enlighten us on these matters.

The scope of this issue is focused on the differential therapeutic effect between relapsing–remitting MS (RRMS) and Progressive MS (PMS). This differance is possibly related to CNS qualitative or quantitative differences in inflammatory phenotypes, e.g., distinct cell subpopulations, cytokines, profile and inflammation sites, as well as in other parameters such as mitochondrial function, iron containment and enzymes profile. Analyzing these inflammatory phenotypes differences may help us to understand why beneficial medications are documented in RRMS but not in PMS, what characteristics underline the few approved PMS medications, and how PMS drugs should be designed.

Prof. Dr. David Naor
Guest Editor

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