After 5-6 years of basic research, the group led by Professor Zhang, Xuan from the Department of Rheumatology and Clinical Immunology,PUMCHfirst reported the pathogenic mechanism of PTEN in systemic lupus erythematosus (SLE), and discovered that the expression and function of B cells in SLE can be restored by regulating miR-7 and PTEN. The relevant thesis was published in the July 23, 2014 issue of Science •Translational Medicine, thus providing new therapeutic targets for SLE.
By analyzing B cells in peripheral blood of newly diagnosed and untreated SLE patients, the group found that several miRNAs, especially miR-7, obstruct the generation of PTEN. Abnormal upregulation of miR-7 will reduce the level of PTEN, thus weakening the effect of negative immunomodulatory effect on B cells. As a result, B cells will be abnormally activated, with abnormal proliferation and apoptosis and producing a large amount of autoantibodies. Through experiments, the group also found that PTEN acts as a “bridge” between miR-7 and B cells. If PTEN is blocked, interference with miR-7 will not produce a regulating effect on B cells. Therefore it was proved that interference with miR-7 and PTEN will serve to restore immunologic functions.
The findings were highly praised by the international academic community.
Science •Translational Medicine published them as a cover story, and the chief editor commented: These data support exploringmiR-7 and PTEN as therapeutic targets for SLE.