Abstract
Neuropsychiatric manifestations are frequently observed in patients with systemic lupus erythematousus (SLE) and are sometimes refractory in clinical practice. Whereas the pathogenicity of neuropsychiatryic SLE (NPSLE) still remains unknown, previous reports indicate that some subsets of autoantibodies (auto Abs) and/or anti-nuclear antibodies (ANA) may be involved in the neuron damage. The majority of NPSLE studies strongly suggested that auto Abs and /or ANA in cerebrospinal fluid (CSF), but not in serum, were important. In anti-N-methyl-D-aspartate receptor 2 (NR2) Abs, which are clearly associated with diffuse NPSLE, an increased permeability of blood-brain barrier is critical for their neurotoxicity. On the other hand, CSF anti-U1 ribonucleoprotein (RNP) Abs, which are useful for NPSLE diagnosis in our study, might be independent of BBB breach and are not specific for diffuse NPSLE. As for other pathogenic auto Abs in for NPSLE, it is well known that anti-ribosomal P and anti-phospholipid Abs are closely associated with lupus psychosis/cognitive dysfunction and cerebrovascular diseases, respectively. Additionally, intrathecal inflammatory mediators (e.g., cytokines) are also important for NPSLE pathogenicity. There are some publications regarding the association between auto Abs and inflammatory mediators. Hopefully, these auto Abs will be recognized not only as a prognostic factor but also as a biomarker for treatment decisions for NPSLE patients in the near future.
