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Regulation of neuroinflammation by B cells and plasma cells
Author(s) -
Wang Angela,
Rojas Olga,
Lee Dennis,
Gommerman Jennifer L.
Publication year - 2021
Publication title -
immunological reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.839
H-Index - 223
eISSN - 1600-065X
pISSN - 0105-2896
DOI - 10.1111/imr.12929
Subject(s) - neuroinflammation , experimental autoimmune encephalomyelitis , immunology , b cell , b cell activating factor , cd20 , regulatory b cells , biology , cytokine , plasma cell , inflammation , antibody
Abstract The remarkable success of anti‐CD20 B cell depletion therapies in reducing the burden of multiple sclerosis (MS) disease has prompted significant interest in how B cells contribute to neuroinflammation. Most focus has been on identifying pathogenic CD20 + B cells. However, an increasing number of studies have also identified regulatory functions of B lineage cells, particularly the production of IL‐10, as being associated with disease remission in anti‐CD20–treated MS patients. Moreover, IL‐10–producing B cells have been linked to the attenuation of inflammation in experimental autoimmune encephalomyelitis (EAE), the animal model of MS. In addition to IL‐10–producing B cells, antibody‐producing plasma cells (PCs) have also been implicated in suppressing neuroinflammation. This review will examine regulatory roles for B cells and PCs in MS and EAE. In addition, we speculate on the involvement of regulatory PCs and the cytokine BAFF in the context of anti‐CD20 treatment. Lastly, we explore how the microbiota could influence anti‐inflammatory B cell behavior. A better understanding of the contributions of different B cell subsets to the regulation of neuroinflammation, and factors that impact the development, maintenance, and migration of such subsets, will be important for rationalizing next‐generation B cell–directed therapies for the treatment of MS.