Scripties UMCG - Rijksuniversiteit Groningen
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CD21-/low B-cells are increased in the auto-inflammatory disease Ankylosing Spondylitis

(2018) Wilbrink, R. (Rick)

Ankylosing Spondylitis (AS) is a chronic inflammatory rheumatic disease mainly affecting the sacroiliac joints and the spine. A well-supported hypothesis suggests that the pathogenesis of AS is driven by cells of the innate immune system. Moreover, the most noticeable mediators are the IL-23/IL-17 axis and tumor necrosis factor (TNF)-α. Current treatment of AS is primarily based on non-steroidal anti-inflammatory drugs (NSAIDs) and disease modifying anti-rheumatic drugs (DMARDs), such as TNF-α inhibitors. B-cells have received little attention regarding their potential role in AS due to the absence of auto-antibodies. In recent years a newly identified B-cell subset, which has a low expression of the molecule cluster of differentiation (CD) 21 expression, has been found to be increased in auto-immune and auto-inflammatory diseases including systemic lupus erythematosus (SLE) and primary Sjogren’s syndrome (pSS), According to previous literature, this particular CD21-/low B-cell subset is thought to be in a state of anergy. This study describes an increased proportion CD21-/low B-cells that express a unique set of immune markers in the blood of AS patients, similar to findings in systemic auto-immune/auto-inflammatory diseases. The similarity in phenotype and increased proportion of CD21-/low B-cells is indicative for B-cell involvement in AS. However, whether CD21-/low B-cells are refractory to B-cell receptor (BCR) stimulation in AS, remains to be solved. Our data analysis does not allow us to draw a firm conclusion on the anergic state of these CD21-/low B-cells in AS.

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