Glomerular histopathology in WT and Psgl-1 −/− mice treated with pristane or PBS for 32 weeks (n = 8 mice per group). Therapies targeting Psgl-1 may be useful in the management of SLE patients at high risk of acute vascular complications although elucidation of downstream pathways will be necessary to identify targets that do not promote nephritis. In conclusion, the increase in stroke size associated with lupus is prevented by Psgl-1 deficiency while nephritis is exacerbated. Infiltration of neutrophils and macrophages at the cerebral infarction site were reduced in pristane-treated Psgl-1−/− mice compared to pristane-treated WT mice. Pristane-treated WT mice showed elevated anti-dsDNA, anti-snRNP, CXCL1, and MCP-1 levels compared to untreated mice however levels of anti-snRNP, MCP-1, and CXCL1 were reduced in pristane-treated Psgl-1−/− mice compared to pristane-treated WT mice. However, stroke size was not increased in pristane-treated Psgl-1−/− mice compared to controls, despite evidence of increased nephritis in Psgl-1−/− mice. Stroke size was increased in pristane-treated WT mice compared to non-pristane-treated WT controls. Stroke was induced following photochemical injury to the middle cerebral artery (MCA). Lupus was induced in female wild-type (WT) and P-selectin glycoprotein ligand-1 deficient (Psgl-1−/−) mice with pristane. Therapies targeting leukocyte recruitment may be beneficial in reducing vascular complications associated with SLE. Systemic lupus erythematosus (SLE) is associated with an elevated risk of vascular complications, including premature stroke.
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