LCN2 and systemic lupus erythematosus: Similar to these findings in MRLlpr/lpr mice, the lack of systemic disease attenuation following deletion of LCN2 in B6.Sle1Sle3 mice suggests that the corrective effects on NP-SLE seen by LCN2 deficiency are primarily the result of brain-specific pathways (17) rather than decreased systemic inflammation or brain-infiltrating T-cells or macrophages.