Differential cytokine changes in myasthenia gravis patients with antibodies against AChR and Musk

Yılmaz, Vuslat; Oflazer, Piraye; Aysal, Fikret; Durmuş, Hacer; Poulos, Kostas; Parman, Yeşim; Tüzün, Erdem; Deymeer, Feza; Saruhan‐Direskeneli, Güher

doi:10.1016/j.jneuroim.2014.08.571

Cited by 9 publications

(19 citation statements)

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“…Mice deficient for the IL‐17 or T‐bet gene, a Th1 transcription factor, were less susceptible to EAMG, as demonstrated by decreases in clinical score, cytokine production, and AChR antibody production . The only 2 studies profiling T cells in MuSK MG mirror the observations in AChR MG, in which CD4 T cells from patients with MuSK MG exhibited enhanced frequencies of Th1 and Th17 cytokines . Highlighting the infancy of study in this field is the fact that the identification of antigen‐specific T cells in MuSK remains to be accomplished.…”

Section: B‐cell‐mediated Mg Immunopathology Influenced By T Cellsmentioning

confidence: 99%

B cells in the pathophysiology of myasthenia gravis

Guptill

Stathopoulos

et al. 2017

Muscle and Nerve

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Myasthenia gravis (MG) is an archetypal autoimmune disease. The pathology is characterized by autoantibodies to the acetylcholine receptor (AChR) in most patients or to muscle-specific tyrosine kinase (MuSK) in others and to a growing number of other postsynaptic proteins in smaller subsets. A decrease in the number of functional AChRs or functional interruption of the AChR within the muscle end plate of the neuromuscular junction is caused by pathogenic autoantibodies. Although the molecular immunology underpinning the pathology is well understood, much remains to be learned about the cellular immunology contributing to the production of autoantibodies. This Review documents research concerning the immunopathology of MG, bringing together evidence principally from human studies with an emphasis on the role of adaptive immunity and B cells in particular. Proposed mechanisms for autoimmunity, which take into account that different types of MG may incorporate divergent immunopathology, are offered. Muscle Nerve 57: 172-184, 2018.

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Section: B‐cell‐mediated Mg Immunopathology Influenced By T Cellsmentioning

confidence: 99%

B cells in the pathophysiology of myasthenia gravis

Guptill

Stathopoulos

et al. 2017

Muscle and Nerve

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“…Several studies have reported changes in cytokine levels in MG patients [26,27]. To further evaluate the role of HLA on cytokine production, selected cytokines were measured in the sera of the disease subgroups that were stratified according to the disease-associated alleles.…”

Section: Cytokines Related To Drb1*14 Drb1*16 or Dqb1*05 In Musk-mg mentioning

confidence: 99%

Relation ofHLA-DRB1to IgG4 autoantibody and cytokine production in muscle-specific tyrosine kinase myasthenia gravis (MuSK-MG)

Çebi

Durmuş

Yılmaz

et al. 2019

Clinical and Experimental Immunology

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A small subset of myasthenia gravis (MG) patients develop autoantibodies against muscle-specific kinase (MuSK), which are predominantly of the immunoglobulin (Ig)G4 isotype. MuSK-MG is strongly associated with HLA-DRB1*14, HLA-DRB1*16 and HLA-DQB1*05. In this study, the possible effects of these HLA associations on MuSK IgG autoantibody or cytokine production were investigated. Samples from 80 MG patients with MuSK antibodies were studied. The disease-associated HLA types were screened in the DNA samples. The IgG1, IgG2, IgG3 and IgG4 titres of the MuSK antibodies and the levels of interleukin (IL)-4, IL-6, IL-17A and IL-10 were measured in the sera. Comparisons were made among the groups with or without HLA-DRB1*14, HLA-DRB1*16 or HLA-DQB1*05. The IgG4 titres of the MuSK antibodies were higher than those of the IgG1, IgG2 and IgG3 isotypes among the whole group of patients. DRB1*14 (+) DRB1*16 (-) patients had higher levels of IgG4 antibodies than those of DRB1*14 (-) DRB1*16 (+) patients. DRB1*14 (+) DRB1*16 (+) patients also had higher levels of IgG4 antibodies than those of DRB1*14 (-) DRB1*16 (+) and DRB1*14 (-) DRB1*16 (-) patients. Higher IL-10 and lower IL-17A levels were measured in DRB1*14 (+) DRB1*16 (-) patients than in DRB1*14 (-) DRB1*16 (-) patients. The higher IgG4 titres of MuSK autoantibodies in patients carrying HLA-DRB1*14 than those in the other patients suggest a role for HLA in the production of the antibodies. The differences in IL-10 and IL-17A support the role of DRB1 in the etiopathogenesis of this autoimmune response.

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“…В качестве посредников они принимают участие в дифференцировке иммунокомпетентных и гемо-поэтических клеток, в формировании механизмов межклеточного взаимодействия, лежащих в осно-ве иммунного ответа. Основная их биологическая активность -регуляция иммунного ответа на всех этапах его развития [117]. В целом следует отметить, что вся эта большая груп-па эндогенных регуляторов участвует в делении и дифференцировке клеток-предшественников функционально активных иммунокомпетентных клеток, изменении экспрессии антигенов и различ-ных маркеров, хемотаксисе, переключении синте-за иммуноглобулинов, индукции цитотоксичности у макрофагов, пролиферации антиген-чувствител ь-ных лимфоцитов, дифференцировке В-клеток в про-дуценты иммуноглобулинов, переключении синтеза иммуноглобулинов с одного изотипа на другой, обе-спечении созревания предшественников цитоток-сических Т-клеток до зрелых эффекторов, индукции цитотоксичности у макрофагов, формировании оча-га воспаления [101,103].…”

Section: роль цитокинов в патогенезе миастении грависunclassified

“…в 2015 г. на экспериментальной моде-ли аутоиммунной миастении показали, что уменьше-ние количества цитокинов коррелирует со снижени-ем уровня антител к ацетилхолиновым рецепторам. Учеными выявлена связь между повышением уровня ФНО-α (фактор некроза опухоли α), интерлейкинами 17А и 21 (ИЛ-17A и ИЛ-21) и тяжестью заболевания с MuSK положительной формой миастении [15,117]. ФНО подавляет активность Т-регуляторных клеток, которые снижают аутореактивность иммунокомпе-тентных клеток, при этом снижение уровня ФНО приводит к восстановлению функции этих кле-ток [55].…”

Section: роль цитокинов в патогенезе миастении грависunclassified

“…При сти-муляции CD40 у пациентов с миастенией были получены значительно более низкие уровни ИЛ-10 и ИЛ-6, чем в группе контроля. При стимуля-ции CD40 и В-клеточного рецептора в дополнение к этим цитокинам также уменьшалось производство ФНО-α [116,117]. Работы Akiyuki Uzawa и соавт.…”

Section: роль цитокинов в патогенезе миастении грависunclassified

See 1 more Smart Citation

Immunopathogenesis of Myasthenia Gravis (Review)

Gasymly¹

2018

Arhivʺ vnutr. med.

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Differential cytokine changes in myasthenia gravis patients with antibodies against AChR and Musk

Cited by 9 publications

References 0 publications

B cells in the pathophysiology of myasthenia gravis

B cells in the pathophysiology of myasthenia gravis

Relation ofHLA-DRB1to IgG4 autoantibody and cytokine production in muscle-specific tyrosine kinase myasthenia gravis (MuSK-MG)

Immunopathogenesis of Myasthenia Gravis (Review)

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