Abstract
Extensive research into ankylosing spondylitis (AS) has suggested the major role of genetics, immune reactions, and the joint–gut axis in its etiology, although an ultimate consensus does not yet exist. The available evidence indicates that both autoinflammation and T-cell-mediated autoimmune processes are actively involved in the disease process of AS. So far, B cells have received relatively little attention in AS pathogenesis; this is largely due to a lack of conventional disease-defining autoantibodies. However, against prevailing dogma, there is a growing body of evidence suggestive of B cell involvement. This is illustrated by disturbances in circulating B cell populations and the formation of auto-reactive and non-autoreactive antibodies, along with B cell infiltrates within the axial skeleton of AS patients. Furthermore, the depletion of B cells, using rituximab, displayed beneficial results in a subgroup of patients with AS. This review provides an overview of our current knowledge of B cells in AS, and discusses their potential role in its pathogenesis. An overarching picture portrays increased B cell activation in AS, although it is unclear whether B cells directly affect pathogenesis, or are merely bystanders in the disease process.
Highlights
Spondyloarthritis (SpA) encompasses a heterogeneous group of related chronic rheumatic immune-mediated diseases, including axial spondyloarthritis, which can be subdivided into ankylosing spondylitis (AS) and non-radiographic axSpA [1]
In recent decades, a growing body of evidence has begun to point towards B cell involvement in the disease process, against prevailing dogma
In AS, the modulation of B cells is illustrated by genetic variation, along with the role of cytokines, such as IL-17 and IL-21, which may directly influence B cell function and development
Summary
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