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吉兰-巴雷综合征中T细胞对髓鞘蛋白的反应。

T cell responses to myelin proteins in Guillain-Barré syndrome.

作者信息

Khalili-Shirazi A, Hughes R A, Brostoff S W, Linington C, Gregson N

机构信息

Department of Neurology, UMDS, London, UK.

出版信息

J Neurol Sci. 1992 Sep;111(2):200-3. doi: 10.1016/0022-510x(92)90069-w.

Abstract

We have investigated the hypothesis that the pathogenesis of Guillain-Barré syndrome (GBS) involves an autoimmune T cell response to P0 and P2 proteins of peripheral nerve myelin. The proliferative responses of blood mononuclear cells (MNC) to myelin proteins and synthetic peptides derived from them were determined in patients with GBS and chronic idiopathic demyelinating polyradiculoneuropathy (CIDP), normal controls (NC) and patients with other neuropathies (ONP). Twelve out of 19 GBS patients responded to P0 or P2, 6 to P0 and its peptides only, 3 to P2 and its peptides only, and 3 to both P0 and P2 antigens. Responses to at least one of the antigens were also found in 6/13 of CIDP patients, but in only 4/17 NC and 2/6 ONP. Immune responses in GBS are heterogeneous. The early T cell responses to P0 protein, described here for the first time, may be important in the pathogenesis of some cases.

摘要

我们研究了如下假说

吉兰-巴雷综合征(GBS)的发病机制涉及针对周围神经髓鞘P0和P2蛋白的自身免疫性T细胞反应。在GBS患者、慢性特发性脱髓鞘性多发性神经根神经病(CIDP)患者、正常对照(NC)以及其他神经病患者(ONP)中,测定了血液单核细胞(MNC)对髓鞘蛋白及其衍生的合成肽的增殖反应。19例GBS患者中有12例对P0或P2有反应,6例仅对P0及其肽有反应,3例仅对P2及其肽有反应,3例对P0和P2抗原均有反应。在13例CIDP患者中的6例也发现了对至少一种抗原的反应,但在17例NC中只有4例,6例ONP中只有2例。GBS中的免疫反应是异质性的。本文首次描述的对P0蛋白的早期T细胞反应可能在某些病例的发病机制中起重要作用。

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