Axial spondyloarthritis (axSpA) is a chronic inflammatory disease that pre-dominantly affects the spine and sacroiliac joints, causing pain, stiffness, and diminished spinal mobility. The immune system is known to play a central role in this disease, and most research has focused on innate immune cells and related inflammatory molecules. In contrast, the role of B cells, a key component of the adaptive immune system, has received comparatively less attention.
This research of Rick Wilbrink aimed to explore the involvement of B cells in the pathogenesis of axSpA. By analyzing peripheral blood samples of patients, changes in specific subsets of B cells, including cells with low or absent expression of the receptor CD21 (CD21lo B cells), were identified. These cells may contribute to the inflammatory process in axSpA by responding to signals from inflammatory environments, and may eventually differentiate into antibody-secreting cells. Interestingly, CD21lo B cells from axSpA patients exhibited a shift towards IgA – an isotype linked to mucosal immunity – pointing to a potential connection between gut and joint inflammation.
Although it remains unclear whether B cells directly drive the disease, their altered frequencies in peripheral blood, altered responsiveness to B cell receptor stimulation, and developmental relationships with antibody-secreting cells indicate their involvement in immune responses of axSpA patients. Understanding the role of B cells in axSpA could open new avenues for treatment, including therapies that target B cells.
