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Role of salivary IgA in the pathogenesis of Sjogren syndrome.

机译:唾液IgA在Sjogren综合征发病机理中的作用。

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摘要

Saliva IgA autoantibodies against M(3) muscarinic acetylcholine receptors (mAChRs) could be a new marker for the diagnosis for Sjogren syndrome (SS) dry mouth. Saliva IgA from dry mouth primary SS (pSS) or secondary SS patients tested by ELISA recognized membrane parotid gland acinar cell antigens and the synthetic 25-mer peptide corresponding to the second extracellular loop of human M(3) mAChRs. Moreover, the IgA fraction was able to inhibit the [(3)H]QNB binding to parotid acinar membrane mAChRs. In addition, the IgA prevented carbachol stimulation of protein secretion by the parotid gland. As controls, IgA and saliva from women without dry mouth and from normal control subjects gave negative results on ELISA, binding, and biological assays, thus demonstrating the specificity of the reaction. IgA autoantibodies against mAChR may be considered among the immunoglobulin factors implicated in the pathophysiology of the development of pSS dry mouth and could be a new marker for differentiating SS dry mouth from non-SS dry mouth.
机译:针对M(3)毒蕈碱乙酰胆碱受体(mAChRs)的唾液IgA自身抗体可能是诊断Sjogren综合征(SS)口干的新标记。唾液IgA来自通过ELISA测试的口干性原发性SS(pSS)或继发性SS患者识别膜腮腺腺泡细胞抗原和对应于人M(3)mAChRs第二个细胞外环的合成25-mer肽。此外,IgA级分能够抑制[(3)H] QNB结合腮腺腺泡膜mAChRs。此外,IgA阻止了腮腺刺激卡巴胆对蛋白质分泌的刺激。作为对照,没有口干的妇女和正常对照组的IgA和唾液在ELISA,结合和生物学分析上均给出阴性结果,从而证明了反应的特异性。抗mAChR的IgA自身抗体可能被认为是与pSS干口发展的病理生理有关的免疫球蛋白因素之一,并且可能是区分SS干口与非SS干口的新标志。

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