MicroRNA-21 deficiency protects from lupus-like autoimmunity in the chronic graft-versus-host disease model of systemic lupus erythematosus.

摘要: MicroRNAs (miRNAs) are small, non-coding RNAs that regulate gene expression primarily at the post-transcriptional level. Emerging evidence supports a regulatory role for miRNAs in immune response and autoimmunity. In this work, we investigated implication of miR-21 experimentally inducible bm12→B6 cGVHD model systemic lupus erythematosus (SLE). host mice deficient show 2-fold reduction splenomegaly, significantly reduced autoantibody titers down-regulated components CD40:CD40L CD28:CD80/86 co-stimulation pathways. Furthermore, demonstrate miR-21-deficient hosts have CD4(+) IL-17(+) cell populations an expanded CD25(+) FoxP3(+) compartment. We propose has pluripotent role, serving to link distinct lymphocyte signaling pathways acting as "rheostat" signals promote B T activation lupus. Collectively, our experiments deficiency is sufficient protect from lupus-like