Fig. 9: Proposed schematic showing new hypothesis for how dysregulated B and T cell interactions could contribute to pathogenesis of JIA-uveitis. | Nature Communications

Fig. 9: Proposed schematic showing new hypothesis for how dysregulated B and T cell interactions could contribute to pathogenesis of JIA-uveitis.

From: Altered B cell activation contributes to the immunopathogenesis of childhood arthritis-associated uveitis

Fig. 9: Proposed schematic showing new hypothesis for how dysregulated B and T cell interactions could contribute to pathogenesis of JIA-uveitis.

Altered B-cell and T-cell interactions could lead to increased GC activation in secondary lymphoid organs, which could lead to an expansion of DN1 B cells in the blood of JIA-uveitis patients. These cells then differentiate into memory B cells, which could then migrate to the uveitic eye and cross the blood-retina barrier. Once in the eye, B cells could differentiate into antibody-producing plasma cells contributing to the general inflammatory milieu and drive chronic inflammation. Future experiments are needed to confirm both the provenance of DN1 B cells and the exact role of GC B cells in EAU pathology. Alternative DN B cell subset trajectories are shown greyed out. Created in BioRender. Jebson, B. (2026) https://BioRender.com/s4ga0th.

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