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格林-巴利综合征患者体内针对磷脂和脑提取物的自身抗体:交叉反应性还是致病性?

Autoantibodies to phospholipids and brain extract in patients with the Guillain-Barre syndrome: cross-reactive or pathogenic?

作者信息

Gilburd B, Stein M, Tomer Y, Tanne D, Abramski O, Chapman Y, Ahiron A, Blank M, Shoenfeld Y

机构信息

Research Unit of Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Israel.

出版信息

Autoimmunity. 1993;16(1):23-7. doi: 10.3109/08916939309010644.

DOI:10.3109/08916939309010644
PMID:8136463
Abstract

Guillain-Barre syndrome (GBS) is a transient neurological disorder characterized by an inflammatory demyelination of peripheral nerves. Although the pathogenesis of GBS has not been elucidated, there is increasing evidence pointing to an autoimmune etiology. We have studied the reactivity of GBS sera with various phospholipids which are known to be important constituents of myelin, and serve as autoantigens in other autoimmune conditions. Sixteen Guillain-Barre syndrome (GBS) sera were studied for the presence of autoantibodies to ssDNA, dsDNA, cardiolipin (CL), phosphatidyl-ethanolamine (PE), phosphatidyl-choline (PC), phosphatidyl-serine (PS), and brain extract. Six of the 16 GBS sera had autoantibodies to one or more of the antigens studied. Three of the sera contained autoantibodies to brain extract (p < 0.05), two of the sera had autoantibodies to dsDNA, ssDNA, CL and PE, and one serum had autoantibodies to PC, and PS. As expected a significant proportion of the lupus sera contained autoantibodies to ssDNA and dsDNA, while the frequency of autoantibodies to different phospholipids was significantly high in sera of patients with systemic lupus erythematosus (SLE) and cerebritis. Absorption of GBS sera with cardiolipin, phosphatidyl-choline, or brain extract inhibited the binding of the sera to cardiolipin. Our results demonstrate that some GBS patients produce autoantibodies to various phospholipid and nuclear antigens. However, these autoantibodies are probably produced as a result of the myelin damage rather than cause the demyelination.

摘要

格林-巴利综合征(GBS)是一种短暂性神经系统疾病,其特征为周围神经的炎性脱髓鞘。尽管GBS的发病机制尚未阐明,但越来越多的证据指向自身免疫病因。我们研究了GBS血清与各种磷脂的反应性,这些磷脂是已知的髓鞘重要组成成分,并且在其他自身免疫性疾病中作为自身抗原。对16份格林-巴利综合征(GBS)血清进行研究,检测其针对单链DNA、双链DNA、心磷脂(CL)、磷脂酰乙醇胺(PE)、磷脂酰胆碱(PC)、磷脂酰丝氨酸(PS)和脑提取物的自身抗体。16份GBS血清中有6份针对一种或多种所研究的抗原有自身抗体。其中3份血清含有针对脑提取物的自身抗体(p<0.05),2份血清针对双链DNA、单链DNA、CL和PE有自身抗体,1份血清针对PC和PS有自身抗体。正如预期的那样,相当比例的狼疮血清含有针对单链DNA和双链DNA的自身抗体,而系统性红斑狼疮(SLE)和脑炎患者血清中针对不同磷脂的自身抗体频率显著较高。用心磷脂、磷脂酰胆碱或脑提取物吸收GBS血清可抑制血清与心磷脂的结合。我们的结果表明,一些GBS患者会产生针对各种磷脂和核抗原的自身抗体。然而,这些自身抗体可能是髓鞘损伤的结果而非导致脱髓鞘的原因。

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