Abstract
Multiple sclerosis (MS) is a frequent autoimmune demyelinating disease of the central nervous system (CNS). There are three clinical forms described: relapsing-remitting multiple sclerosis (RRMS), the most common initial presentation (85%) among which, if not treated, about half will transform, into the secondary progressive multiple sclerosis (SPMS) and the primary progressive MS (PPMS) (15%) that is directly progressive without superimposed clinical relapses. Inflammation is present in all subsets of MS. The relapsing/remitting form could represent itself a particular interest for the study of inflammation resolution even though it remains incomplete in MS. Successful resolution of acute inflammation is a highly regulated process and dependent on mechanisms engaged early in the inflammatory response that are scarcely studied in MS. Moreover, recent classes of disease-modifying treatment (DMTs) that are effective against RRMS act by re-establishing the inflammatory imbalance, taking advantage of the pre-existing endogenous suppressor. In this review, we will discuss the active role of regulatory immune cells in inflammation resolution as well as the role of tissue and non-hematopoietic cells as contributors to inflammation resolution. Finally, we will explore how DMTs, more specifically induction therapies, impact the resolution of inflammation during MS.
Highlights
Multiple sclerosis (MS) is a frequent autoimmune demyelinating disease of the central nervous system (CNS)
Auto reactive CD4+ T cells are activated in the periphery and cross the blood-brain barrier to reach the CNS, known as the
Once in the CNS, CD4+ T cells are reactivated by local antigen presenting cells, which will trigger an inflammatory reaction, inducing the recruitment of other leukocytes
Summary
Multiple sclerosis (MS) is a frequent autoimmune demyelinating disease of the central nervous system (CNS). There is no documentation that crossing the blood-brain barrier could skew leukocytes toward an anti-inflammatory phenotype but the choroid plexus could be considered as a selective gate, facilitating the passage of regulatory cells to the CNS [129] Once they have crossed the BCSFB, immune cells reach to cerebrospinal fluid that itself is a suppressive environment [130]. Corticosteroids have robust anti-inflammatory properties [139], such as induction of T cell apoptosis and inhibition of BBB disruption They further play an active role in the resolution of inflammation as they increase regulatory T (Treg) number and enhance their suppressive capacities [140].
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