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Decreased mRNA expression of TNF‐α and IL‐10 in non‐stimulated peripheral blood mononuclear cells in myasthenia gravis
Author(s) -
Huang W.X.,
Huang P.,
Fredrikson S.,
Pirskanen R.,
Hillert J.
Publication year - 2000
Publication title -
european journal of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 124
eISSN - 1468-1331
pISSN - 1351-5101
DOI - 10.1046/j.1468-1331.2000.00056.x
Subject(s) - myasthenia gravis , peripheral blood mononuclear cell , medicine , tumor necrosis factor alpha , cytokine , autoantibody , endocrinology , immunology , messenger rna , acetylcholine receptor , interleukin , stimulation , receptor , in vitro , antibody , biology , gene , biochemistry
Myasthenia gravis (MG) is characterized by T cell‐dependent autoantibodies to the acetylcholine receptor on the post‐synaptic membrane of the neuromuscular junction. The production of autoantibodies is regulated by T cells via cytokines. To investigate the involvement of interferon gamma (IFN‐γ), tumour necrosis factor alpha (TNF‐α), interleukin‐4 (IL‐4) and interleukin‐10 (IL‐10) in MG, the mRNA levels of these cytokines in peripheral blood mononuclear cells without stimulation in vitro were quantified by competitive reverse transcription polymerase chain reaction technique. The mRNA level of TNF‐α was significantly lower ( P = 0.0004) in the overall group of MG patients compared with controls. IL‐10 was also lower in MG patients ( P = 0.008), most markedly in non‐thymectomized patients ( P = 0.016). There were no significant differences in IFN‐γ and IL‐4 between patients and healthy controls, but the mRNA levels of IL‐4 in non‐thymectomized patients was significantly lower than in controls ( P = 0.02) and in thymectomized patients ( P = 0.03). These results, reflecting the in vivo expression pattern of these cytokines in the periphery, suggest an altered cytokine expression at the systemic level in MG.