IL36A and lupus nephritis: Importantly, significant upregulation of these three markers did not occur in the human biopsies [10], indicating a lesser degree of tubular damage in treated individuals; this is consistent with our previous findings that glomerular damage precedes tubulointerstitial damage in NZB/W mice, that upregulation of LCN-2 and HAVCR1 occurs only in the late stages of SLE nephritis in NZB/W and NZW/BXSB mice, and that there is marked downregulation of LCN-2, IL1F6 and HAVCR1 in the kidneys of mice in remission ([11], and manuscript in preparation).