Myasthenia gravis-specific aberrant neuromuscular gene expression by medullary thymic epithelial cells in thymoma

Yasumizu, Yoshiaki; Ohkura, Naganari; Murata, Hisashi; Kinoshita, Makoto; Funaki, Soichiro; Nojima, Satoshi; Kido, Kansuke; Kohara, Masaharu; Motooka, Daisuke; Okuzaki, Daisuke; Suganami, Shuji; Takeuchi, Eiichi; Nakamura, Yurika; Takeshima, Yusuke; Arai, Mamoru; Tada, Satoru; Okumura, Meinoshin; Morii, Eiichi; Shintani, Yasushi; Sakaguchi, Shimon; Okuno, Tatsusada; Mochizuki, Hideki

doi:10.1101/2021.12.19.473411

Cited by 2 publications

(2 citation statements)

References 72 publications

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“…Also, the antigenicity of exogenous molecules (e.g., a microbial protein) with significant homology with a host protein or host-derived endogenous protein associated with cell stress or cell damage is believed to act as an autoantigen to trigger such onset of the autoimmune response (25). A recent study of single-cell RNA sequencing analysis detected viral transcripts for Epstein-Barr virus and herpesvirus 6A in the thymoma of MG patients; however, the correlation with the virus was nonsignificant (26). Thus, the exact mechanism underlying the steps of immune activation in the thymus, contributed by infection and inflammation, is incompletely understood.…”

Section: Role Of Infection and Inflammation In Mg Etiologymentioning

confidence: 99%

Inflammation and autoimmune myasthenia gravis

Huda

2023

Front. Immunol.

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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.

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Section: Role Of Infection and Inflammation In Mg Etiologymentioning

confidence: 99%

Inflammation and autoimmune myasthenia gravis

Huda

2023

Front. Immunol.

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“…Thymoma accounts for approximately 95% of all thymic tumors (2, 3). Patients with thymoma show complications with various diseases (4), among which myasthenia gravis (MG) is the most common (5,6). MG involves skeletal muscles of the whole body, and its main clinical characteristics are the volatility of aggravation after exercise and reduction after rest.…”

Section: Introductionmentioning

confidence: 99%

Identification of cytokines in benign and malignant thymus tumors: based on Mendelian randomization and proteomics

Zhu,

Shi,

Yang

et al. 2024

Front. Endocrinol.

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ObjectiveThe aim of this study was to identify potential causal cytokines in thymic malignancies and benign tumors from the FinnGen database using Mendelian randomization (MR).MethodsIn this study, data from genome-wide association studies (GWAS) of 91 cytokines were used as exposure factors, and those of thymic malignant tumors and thymic benign tumors were the outcome variables. Two methods were used to determine the causal relationship between exposure factors and outcome variables: inverse variance weighting (IVW) and MR-Egger regression. Sensitivity analysis was performed using three methods, namely, the heterogeneity test, the pleiotropy test, and the leave-one-out test.ResultsThere was a causal relationship between the expression of fibroblast growth factor 5, which is a risk factor for thymic malignant tumors, and thymic malignant tumors. C-C motif chemokine 19 expression, T-cell surface glycoprotein CD5 levels, and interleukin-12 subunit beta levels were causally related to thymic malignant tumors and were protective. Adenosine deaminase levels, interleukin-10 receptor subunit beta expression, tumor necrosis factor (TNF)-related apoptosis-inducing ligand levels, and TNF-related activation-induced cytokine levels showed a causal relationship with thymic benign tumors, which are its risk factors. Caspase 8 levels, C-C motif chemokine 28 levels, interleukin-12 subunit beta levels, latency-associated peptide transforming growth factor beta 1 levels, and programmed cell death 1 ligand 1 expression showed a causal relationship with thymic benign tumors, which are protective factors. Sensitivity analysis showed no heterogeneity.ConclusionCytokines showed a causal relationship with benign and malignant thymic tumors. Interleukin-12 subunit beta is a common cytokine that affects malignant and benign thymic tumors.

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Myasthenia gravis-specific aberrant neuromuscular gene expression by medullary thymic epithelial cells in thymoma

Cited by 2 publications

References 72 publications

Inflammation and autoimmune myasthenia gravis

Inflammation and autoimmune myasthenia gravis

Identification of cytokines in benign and malignant thymus tumors: based on Mendelian randomization and proteomics

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