AI Article Synopsis
- Myasthenia gravis (MG) is an autoimmune disease that causes muscle weakness and fatigue due to the body attacking its own neuromuscular junctions.
- The study explored the impact of an IL-6 receptor (IL-6R) antibody treatment in a mouse model of MG, finding that it helped improve muscle strength and reduced harmful autoantibodies.
- Results also indicated that IL-6R antibody treatment led to a decrease in specific immune cells linked to MG, suggesting it could be a promising new therapy for the condition.
Article Abstract
Myasthenia gravis (MG) is a chronic autoimmune disease characterized by muscle weakness and fatigue. It is caused by pathological autoantibodies against components expressed at neuromuscular junctions, such as acetylcholine receptor (AChR). Interleukin-6 (IL-6) has been suggested to play a role in the pathogenesis of MG, and IL-6 receptor (IL-6R) antibody treatment may provide a novel therapeutic option. In this study, we investigated the effects of IL-6R antibody treatment in an experimental autoimmune MG (EAMG) mouse model. We demonstrated that IL-6R antibody treatment improved muscle weakness, reduced IgG deposition at neuromuscular junctions, and the levels of AChR autoantibodies in serum. In addition, follicular helper T cells and Th17, plasma cells in lymph nodes were lower in IL-6R antibody treated mice. Our findings suggest that IL-6R blockade may be a novel and effective therapeutic strategy for the treatment of MG.
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Source |
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11094227 | PMC |
| http://dx.doi.org/10.3389/fneur.2024.1356300 | DOI Listing |
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