Inflammation and autoimmune myasthenia gravis

Abstract

Myasthenia gravis (MG) is a neuromuscular autoimmune disorder characterized by chronic but intermittent fatigue of the eye- and general body muscles. Muscle weakness is caused primarily by the binding of an autoantibody to the acetylcholine receptors, resulting in blockage of normal neuromuscular signal transmission. Studies revealed substantial contributions of different proinflammatory or inflammatory mediators in the pathogenesis of MG. Despite these findings, compared to therapeutic approaches that target autoantibody and complements, only a few therapeutics against key inflammatory molecules have been designed or tested in MG clinical trials. Recent research focuses largely on identifying unknown molecular pathways and novel targets involved in inflammation associated with MG. A well-designed combination or adjunct treatment utilizing one or more selective and validated promising biomarkers of inflammation as a component of targeted therapy may yield better treatment outcomes. This review briefly discusses some preclinical and clinical findings of inflammation associated with MG and current therapy approaches and suggest the potential of targeting important inflammatory marker(s) along with current monoclonal antibody or antibody fragment based targeted therapies directed to a variety of cell surface receptors.

An increase in fibrinogen levels despite plasma exchange in a myasthenia gravis patient; a case report

“…Patients with acute inflammation can present with constant elevation in fibrinogen levels. A recent article has shown that proinflammatory and inflammatory mediators play a significant role in the pathogenesis of MG [4]. We demonstrated that the level of fibrinogen, which is often thought to be a limiting factor in the continuation of plasmapheresis due to the risk of bleeding, may not be a reliable indicator of adequate blood clotting.…”

A new gene signature associated with disulfidptosis that forecasts myasthenia gravis and suggests infiltration of immune microenvironment in thymoma patients

“…Besides B cells, which are the main contributors to the production of autoantibodies, T lymphocyte subsets, particularly T helper cells, also have a vital function in TAMG. T helper cells have the ability to start and maintain long-lasting inflammation, enhance inflammatory signals, influence class switching and somatic hypermutation, and transform B cells into plasma cells that generate autoantibodies [ 11 ]. Ultimately, these processes result in the growth and advancement of MG.…”

“…Currently, the precise understanding of TAMG remains uncertain, although scientists theorize that either the tumor cells or the atypical immune cells in the thymus gland might initiate an immune reaction against AChR or other elements of the neuromuscular junction [ [9] , [10] , [11] ]. The overexpression of specific genes has been linked to TAMG, and the reduced expression of CTLA-4 in thymoma could potentially heighten the vulnerability to developing MG [ 12 , 13 ].…”

Systemic Inflammatory Response Index, a Potential Inflammatory Biomarker in Disease Severity of Myasthenia Gravis: A Pilot Retrospective Study

“… 2 While the involvement of inflammatory processes in MG is well-established, therapeutic options specifically targeting key inflammatory molecules remain limited, with only a handful reaching clinical trials. 3–5 This underlines the critical need for identifying novel biomarkers associated with the inflammatory response, which could potentially pave the way for more effective and targeted therapeutic strategies in MG.…”