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Review
. 2018 Nov 10;9(1):9.
doi: 10.1007/s13317-018-0109-x.

Regulatory B and T lymphocytes in multiple sclerosis: friends or foes?

Georgios K Vasileiadis  1 , Efthymios Dardiotis  2 , Athanasios Mavropoulos  3 , Zisis Tsouris  1 , Vana Tsimourtou  1 , Dimitrios P Bogdanos  3 , Lazaros I Sakkas  3 , Georgios M Hadjigeorgiou  1   4
Affiliations
Review

Regulatory B and T lymphocytes in multiple sclerosis: friends or foes?

Georgios K Vasileiadis et al. Auto Immun Highlights. .

Abstract

Current clinical experience with immunomodulatory agents and monoclonal antibodies in principle has established the benefit of depleting lymphocytic populations in relapsing-remitting multiple sclerosis (RRMS). B and T cells may exert multiple pro-inflammatory actions, but also possess regulatory functions making their role in RRMS pathogenesis much more complex. There is no clear correlation of Tregs and Bregs with clinical features of the disease. Herein, we discuss the emerging data on regulatory T and B cell subset distributions in MS and their roles in the pathophysiology of MS and its murine model, experimental autoimmune encephalomyelitis (EAE). In addition, we summarize the immunomodulatory properties of certain MS therapeutic agents through their effect on such regulatory cell subsets and their relevance to clinical outcomes.

Keywords: Autoimmunity; Demyelination; Immunity; Regulation.

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Conflict of interest statement

Conflict of interest

None.

Human and animal rights

This article does not contain any studies with animals performed by any of the authors.

Informed consent

This article does not require informed consent due to the lack of human participants.

Figures

Fig. 1
Fig. 1
Typical flow cytometric analysis of memory and transitional Bregs in RRMS. PBMCs from representative patients with RRMS at diagnosis, relapse and remission were stained with CD19, CD24, CD27 and CD38 moAbs and analyzed by flow cytometry. Total lymphocytes were gated based on forward-side scatter characteristic excluding dead cells and debris (gate R1). Transitional Bregs were identified based on high expression of CD38 and CD24 markers (green color—gate R2) and positivity for CD19. Memory Bregs were identified based on high expression of CD24, positivity for CD19, CD27 markers and lack of CD38 expression (blue color—gate R3). At remission, transitional Bregs appear significantly increased
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