Ariel Rechtman
(Credit: LinkedIn)
Newly published findings in Frontiers in Immunology showed lower soluble CD83 (sCD83) levels in patients with neuromyelitis optica spectrum disorders (NMOSD) and those with relapsing myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), suggesting sCD83 as a potential prognostic biomarker for these diseases. In contrast, results showed an increase in sCD83 levels after IVIG and immunosuppressive therapy, potentially reflecting either a direct effect of the treatment or a compensatory rebound response following immune suppression.1
Researchers enrolled 231 untreated participants into the study, which included 64 patients with MOGAD, 56 patients with NMOSD, 47 patients with MS, and 64 healthy controls (HCs). Findings in the peripheral blood mononuclear cells (PBMCs) analysis revealed that sCD83 levels were lower in NMOSD compared with MOGAD (0.44 [±0.22] RQ vs 1.16 [±0.92] RQ, P = .02) and HCs (0.44 [±0.22] RQ vs 1.07 [±0.91] RQ, P = .05). Notably, patients with NMOSD had a reduced sCD83/CD83 expression ratio compared with HCs (0.71 [±0.16] vs 1.04 [±0.48], P = .02), patients with MOGAD (0.71 [±0.16] vs 1.02 [±0.39], P = .04), and those with MS (0.71 [±0.16] vs 1.16 [±0.45], P = .006).
“In conclusion, our study consistently identified lower sCD83 levels in NMOSD patients compared to those with MOGAD and HCs,” lead author Ariel Rechtman, a PhD student in Medical Bioscience at Hebrew University, and colleagues wrote.1 “These findings highlight sCD83 as a promising biomarker for assessing disease severity, treatment response and early signs of disease activation. Given the risk of irreversible neurological damage associated with relapses, a rapidly responsive biomarker like sCD83 could aid timely therapeutic decision-making. Collectively, our results support sCD83 as both a therapeutic target and a biomarker in CNS demyelinating diseases.”
In an attempt to assess CD83 expression in patients with NMOSD and those with MOGAD as well as its correlation with disease activity, researchers extracted RNA from PBMCs of each group of participants and then analyzed their CD83 expression levels. Authors then used ELISA to quantify sCD83 levels in the cerebrospinal fluid (CSF) and serum of the groups of patients. In addition, researchers evaluated the impact of therapeutic agents used for central nervous system demyelinating diseases on sCD83 expression levels.
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In the CSF analysis, NMOSD had significantly lower sCD83 levels compared with MOGAD (215.20 [±202.80] pg/mL vs 44.77 [±47.84] pg/mL, P = .02) and other noninflammatory neurological disorders (311.30 [±411.80] pg/mL vs 44.77 [±47.84] pg/mL, P = .002). Furthermore, sCD83 expression was significantly lower in patients with relapsing MOGAD compared with those with monophasic disease (0.62 [±0.60] RQ vs 1.36 [±1.03] RQ, P = .04). Similarly, sCD83 levels in the sera were significantly reduced in relapsing patients compared with those with the monophasic form (3049.57 [±4621.34] pg/mL vs 10694.80 [±9846.70] pg/mL, p = 0.0009).
Additional findings displayed a significant positive correlation between serum sCD83 levels and normalized total brain volume of patients with MOGAD (r = 0.66, P = .0004). Researchers also reported a significant negative correlation between serum sCD83 levels and the visual evoked potential (VEP) score2 in patients with NMOSD who had optic neuritis (n = 27; r = -0.50, P = 0.00). Moreover, IVIG significantly increased sCD83 concentrations in the serum of those with MOGAD and NMOSD (n = 12, from 3650.21 [±6523.94] pg/mL to 9937.99 [±11710.02] pg/mL, P = .002).
“Limitations of this study include the relatively small number of participants, which can be attributed to the rarity of these disorders. Another limitation is that different treatments can affect sCD83 levels in varying ways; therefore, serum samples intended for disease monitoring should be collected prior to the initiation of therapy,” Rechtman et al noted.1 “Further research with larger cohorts is necessary to validate the use of sCD83 as a biomarker for CNS antibody-mediated demyelinating disease severity and as a potential therapeutic target for these disorders.”