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DNA damage responses drive the autoreactivity of B cells

B cells in lupus erythematosus patients exhibit an autoreactive phenotype characterized by excessive activation and antibodies production. We reveal that ATR-mediated DNA damage response (DDR) drives the pathogenicity of B cell responses in SLE. Pharmacological targeting of ATR, attenuated B-cell immunogenic profile, proposing DDR as a novel therapeutic target.


Pathogenic bacteria inhibit host cell secretion to manipulate host immunity

Some phytopathogenic bacteria produce an effector protein that inhibits exocytosis by affecting the proper assembly of the exocyst complex.
Under normal conditions (A), the exocyst complex is properly assembled to transfer the secretory vesicles to the cell membrane for the secretion their content into the apoplast.
When the cell is infected by the bacterium Xanthomonas (B), an effector protein blocks the proper assembly of the exocyst complex, thereby inhibiting the process of extracellular secretion.

[Press Release]  [Plant Cell]