Association of antibodies against myelin and neuronal antigens with neuroinflammation in systemic lupus erythematosus

Abstract

Anti-NS antibodies, most prevalently anti-MOG antibodies, are significantly associated with NPSLE and manifest with the distinct neurological syndrome associated with the antibody in a subgroup. Follow-up studies in large, independent cohorts will reveal whether these anti-NS antibodies could serve as a diagnostic and prognostic biomarker for NPSLE and enable tailored treatment decisions in this challenging and diverse patient cohort.

Aquaporin-4-IgG positive neuromyelitis optica spectrum disorder and systemic autoimmune diseases overlap syndrome: a single-center experience

“…Overall, AQP4-IgG antibodies have been detected in 0.6-3% and 10% of SLE and pSS cohorts, respectively. [23][24][25] Nowadays, several studies have proven the high syndrome specificity of AQP4-IgG antibodies, as these autoantibodies have not been detected in sera of patients with SLE/pSS without NMOSD features. 18,23,25,26 Pittock et al reported that only SLE/pSS patients with NMOSD clinical syndromes were AQP4-IgG seropositive in an American and a French cohort.…”

Systemic lupus erythematosus: year in review 2019

“…The Swiss SLE Cohort Study Group demonstrated that antibodies against components of nervous system were found in 13% (23/174) of total SLE populations, and anti-myelin oligodendrocyte glycoprotein antibody was significantly associated with NP-SLE. [ 28 ] Besides, some classic antibodies, such as anti-phospholipid, anti-ribosomal P, and anti-aquaporin 4 antibodies are implicated in NP-SLE. Nevertheless, no gold standard has been established for the diagnosis of NP-SLE so far.…”

Autoantibodies against Neurologic Antigens in Nonneurologic Autoimmunity

“…In AQP4 autoantibody–positive NMOSD, autoantibodies that relate to SLE such as ANA and dsDNA are frequently encountered (17). In SLE, AQP4 autoantibodies and concurrent NMOSD manifestations are also reported (36, 37, 41, 42). Importantly, AQP4 autoantibodies have been found to be present in the peripheral blood of SLE patients or in a single healthy individual, both without clinical evidence of NMOSD or CNS involvement (37, 43, 44); in the case of the healthy individual, NMOSD became clinically manifested 10 y later.…”

“…In SLE, AQP4 autoantibodies and concurrent NMOSD manifestations are also reported (36, 37, 41, 42). Importantly, AQP4 autoantibodies have been found to be present in the peripheral blood of SLE patients or in a single healthy individual, both without clinical evidence of NMOSD or CNS involvement (37, 43, 44); in the case of the healthy individual, NMOSD became clinically manifested 10 y later. For disease to manifest, it may be that a second event induces blood-brain barrier permeability to allow serum AQP4 IgG and/or AQP4 autoantibody–expressing B cells to enter the CNS (45, 46).…”

“…A broader reduction of self-tolerance in SLE would be congruous with mildly increased alternate autoimmunity, defined by the presence of at least one autoantibody primarily associated with another autoimmune disease, in SLE compared with RA and T1D (35). Moreover, patients with SLE have been known to harbor Abs against various nervous system Ags with or without associated clinical comorbidity (36, 37). In contrast, examination of B cell tolerance with an assay that was used to establish human central (bone marrow) and peripheral (blood) tolerance checkpoints does indicate similar loss of tolerance across different autoimmune diseases including SLE, RA, and T1D (38–40).…”