CXCL9 and systemic lupus erythematosus: In conclusion, our results suggest that in situ LN cellular and molecular irregularities characterized by i) sustained type I IFN signaling, ii) potent inflammatory signals (e.g., IL-21 and chemokines like CXCL9-CXCL11) iii) impaired generation of PD1hiCD57hiGATA3hi TFH cells and IL4-signaling and iv) accumulation of extrafollicular, potentially autoreactive, ABCs, could play an important role for the loose of tolerance and the generation of autoantibodies in SLE.