Lack of Ets1 Gene Leads to SLE (IMAGE)
Caption
(Left) IBS/POSTECH researchers discovered that the deletion of the Ets1 gene in certain immune cells (gray) leads to increased expression of T follicular helper type 2 (Tfh2) genes (Bcl6, CXCR5, IL4ra). (Middle) This leads to expansion of the Tfh2 cells population (green). In secondary lymphoid organs, such as lymph nodes and the spleen, Tfh2 interacts and activates antibody-producing cells (B cells, in blue). Once activated, B cells mature into autoantibody secreting plasma cells (PC). (Right) Autoantibodies attack organs, such as the skin and kidney, causing medical complications, such as malar rash and nephritis. An increase in Tfh2 cells is correlated with an increase in disease severity and autoantibodies levels. Interestingly, the IBS/POSTECH research team found that blocking IL4 could improve the disease outcome, in particular they observed a reduction in spleen size and in number of autoantibodies-producing cells after treating SLE mice with anti-IL4. (Adapted from Kim CJ et al, Immunity, 2018).
Credit
(Adapted from Kim CJ et al, <em>Immunity</em>, 2018).
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