Clinical Neurology: Research Article
Wang M. · Xia D. · Sun L. · Bi J. · Xie K. · Wang P.Introduction: The purpose of this study was to analyze IL-33 maybe as a biomarker especially with respect to intrathecal immunoglobulin (IgG) synthesis which was involved in the immune -mediated process in the demyelinating disease of the central nervous system. Methods: We aimed to determine the risk association of the serum and CSF levels of IL-33 in AQP4+NMOSD patients and MOGAD patients compared with the control group. Levels of inflammatory (IL-2,IL-4,IL-6 and IL-10) markers and QAlb, the IgG index and 24-hour IgG synthesis rate were assessed in 28 AQP4+NMOSD patients and 11 MOGAD patients. Disease severity was assessed using the Expanded Disability Status Scale (EDSS). Results: The level of IL-33 in serum decreased firstly but then increased gradually in AQP4+NMOSD and MOGAD. The serum level of lL-2, IL-4 and IL-10 increased more significantly and decreased more rapidly after MP treatment. The level of IL-33 in CSF increased progressively in AQP4+NMOSD and MOGAD, especially in MOGAD. The QAlb levels were increased significantly in the CSF of MOGAD patients and AQP4+NMOSD patients on the acute stage of the disease. The IgG index and 24-hour IgG synthesis rate were also increased significantly in the CSF of two groups similarly. Conclusions: Thus, we concluded that IL-33 may induce dysfunction of the blood brain barrier and lead to intrathecal synthesis of immunoglobulin in the AQP4+NMOSD and MOGAD, especially in MOGAD. It maybe as a biomarker, at least in part, was involved in the demyelinating diseases of the central nervous system.
The Author(s). Published by S. Karger AG, Basel
Article / Publication Details Open Access License / Drug Dosage / Disclaimer This article is licensed under the Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC). Usage and distribution for commercial purposes requires written permission.
留言 (0)