In line with recent reports regarding the role of pDCs in SLE-prone animals25, 26, 27, our findings further suggests that the Siglec-H-mediated control of pDC function is crucial for the IFN-I-dependent progression of lupus-like disease as manifested by the impact on anti-self NA Ab production and glomerulonephritis. Here, XK is linked to glomerulonephritis.