Figure 2.

Implication of IFN-β in thymic changes associated with EOMG. IFN-β induces the expression of ⍺-AChR by TEC but tends also to induce TEC death. This could lead to the capture of TEC proteins, including the ⍺-AChR, by DC favoring an initial cross-presentation and autoreactivity toward ⍺-AChR. In parallel, IFN-β induces the expression of CXCL13 and CCL21, chemokines leading to the recruitment of peripheral B cells, and ectopic germinal center development. Germinal centers allow the maturation of autoreactive AChR B cells and their survival might be favored by BAFF that is overexpressed by TEC in response to IFN-β. Next, thymic myoid cells presenting AChR at their surface could be the first target of anti-AChR antibodies exacerbating the autoimmune reaction. IFN-β also induces pro-inflammatory cytokines such as IL-23 favoring the differentiation of naive T cells into pro-inflammatory Th17 cells that produce IL-17. Altogether, this demonstrates that IFN-β is a key orchestrator of thymic changes in EOMG.