Central role of interferon-beta in thymic events leading to myasthenia gravis

Clinical features and impact of myasthenia gravis disease in Australian patients

“…Infections have been proposed to trigger autoimmunity through molecular mimicry [20,21] and there have been suggestions that MG arises through cross-reactivity between infectious agents and the AChR. However, it has also been suggested that viral infections can trigger MG disease by a proinflammatory process in the thymus [22] with increased interferon beta expression [23]. The wide range of precipitating events reported by our patients suggests that the disease trigger is non-specific.…”

Thymic B cells promote thymus-derived regulatory T cell development and proliferation

“…Thymic B cells present peptides derived from autoantigens captured by their B-cell receptors (BCRs) and potentially eliminate auto-reactive thymocytes [19]. This view is exemplified by the finding that MOG [35][36][37][38][39][40][41][42][43][44][45] peptide presenting thymic B cells have been shown to induce the deletion of MOG-specific T cells in the thymus of B MOG /2D2 mice [20]. These data demonstrate that thymic B cells contribute to the negative selection of self-reactive thymocytes.…”

Autoimmune Thyroiditis and Myasthenia Gravis

“…IFN-I, especially IFN-β, could play a central role in the thymic follicular hyperplasia of MG patients by inducing high expression of α-AChR and of CXCL13 chemokine in thymic epithelial cells, and of the chemokine CCL21 in endothelial lymphatic cells, two chemokines involved in the abnormal recruitment of B cells in EOMG thymuses. IFN-β also increases B-cell activating factor expression, which promotes the development of autoreactive B cells (48). Also, IFN-β overexpression in MG thymus can mediate the effects of dsRNA activation and causes α-AChR subunit overexpression, suggesting that IFN-β can play a central role in MG development (36).…”