Table 2. Potentially relevant autoantibodies in neuropsychiatric SLE.

GAPDH: Glyceraldehyde 3-phosphate dehydrogenase, ab: antibody, SBSN: supra-basin, CSF, cerebrospinal fluid, BC RNA: brain cytoplasmic ribonucleic acid, CNS: central nervous system.

Autoantibody	Induction	Clinical finding
Anti-GAPDH Ab [26]	Induce neurite interaction and impairment of neuronal plasticity by blocking and binding of synaptic molecules.	Antibody level increases in SLE and NPSLE and is associated with generalized disease activity, cognitive dysfunction, and psychiatric manifestations.
Anti-SBSN Ab [27]	Astrocytes exposed to antibodies have altered senescence and autophagy pathways.	It can be a helpful marker to differential NPSLE from SLE in the absence of NP symptoms because anti-SBSN antibody and the associated immune complex were only detected in the CSF of NPSLE.
Anti-UCH-L1 Ab [28]	Detected in the CSF of NPSLE patients and has been prosed as a potential biomarker of NPSLE.	NPSLE patients had significantly increased levels of CSF anti-UCH-L1. In addition, this marker was associated with enhanced disease severity and generalized disease activity.
Anti-BC RNA [29]	Responsible for diminished delivery of BC RNA to synaptodendritic sites in the brain.	Lack of BC RNA in CNS causes phenotypic abnormalities and cognitive decline.