Present understanding in the matter is that multiple interrelated mechanisms attributed to underlie SLE-related brain damage include blood-brain barrier dysfunction, vascular inflammation, thrombosis, vascular occlusion caused by atherosclerotic changes, neuroendocrine imbalance, tissue and neural damage mediated by autoantibodies (such as anti-ribosome P0 antibody, ACL), and proinflammatory factors (such as IL-1, IL-6, IL, 8, and TNF-α) combine to produce neuronal loss [50–53]. Here, IL6 is linked to systemic lupus erythematosus.