IL4 and systemic lupus erythematosus: Together with the PD-L1 overexpression by blood basophils from SLE patients (Fig. 1e), these results strongly suggest that, as demonstrated in the lupus-like mouse models (Figs. 2–8), basophils promote the pathogenic accumulation of TFH and TFH2 cells during SLE pathogenesis through their expression of PD-L1 and IL-4.