Subsequently, we showed that endothelial-specific disruption of HS modifying enzyme N-deacetylase/sulfotransferase (NDST-1) reduced PMN influx during anti-GBM-induced glomerulonephritis, whereas silencing of NDST-1 in cultured glomerular endothelial cells reduced L-selectin, CXCL1, CXCL2 and CCL2 binding in vitro as well [20]. Here, SELL is linked to glomerulonephritis.