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感染HIV的个体中存在的抗糖脂抗体能引发免疫性脱髓鞘吗?

Can antiglycolipid antibodies present in HIV-infected individuals induce immune demyelination?

作者信息

Petratos S, Gonzales M E

机构信息

Walter and Eliza Hall Institute of Medical Research, Department of Anatomical Pathology, Royal Melbourne Hospital, Parkville, Victoria, Australia.

出版信息

Neuropathology. 2000 Dec;20(4):257-72. doi: 10.1046/j.1440-1789.2000.00356.x.

DOI:10.1046/j.1440-1789.2000.00356.x
PMID:11211050
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7167963/
Abstract

Of the eight clinically defined neuropathies associated with HIV infection, there is compelling evidence that acute and chronic inflammatory demyelinating polyneuropathy (IDPN) have an autoimmune pathogenesis. Many non-HIV infected individuals who suffer from sensory-motor nerve dysfunction have autoimmune indicators. The immunopathogenesis of demyelination must involve neuritogenic components in myelin. The various antigens suspected to play a role in HIV-seronegative IDPN include (i) P2 protein; (ii) sulfatide (GalS); (iii) various gangliosides (especially GM1); (iv) galactocerebroside (GalC); and (v) glycoproteins or glycolipids with the carbohydrate epitope glucuronyl-3-sulfate. These glycoproteins or glycolipids may be individually targeted, or an immune attack may be raised against a combination of any of these epitopes. The glycolipids, however, especially GalS, have recently evoked much interest as mediators of immune events underlying both non-HIV and HIV-associated demyelinating neuropathies. The present review outlines the recent research findings of antiglycolipid antibodies present in HIV-infected patients with and without peripheral nerve dysfunction, in an attempt to arrive at some consensus as to whether these antibodies may play a role in the immunopathogenesis of HIV-associated inflammatory demyelinating polyneuropathy.

摘要

在与HIV感染相关的8种临床定义的神经病变中,有确凿证据表明急性和慢性炎症性脱髓鞘性多发性神经病(IDPN)具有自身免疫发病机制。许多患有感觉运动神经功能障碍的非HIV感染个体都有自身免疫指标。脱髓鞘的免疫发病机制必定涉及髓鞘中的神经源性成分。怀疑在HIV血清阴性的IDPN中起作用的各种抗原包括:(i)P2蛋白;(ii)硫脂(半乳糖硫酸酯);(iii)各种神经节苷脂(尤其是GM1);(iv)半乳糖脑苷脂(GalC);以及(v)带有碳水化合物表位葡糖醛酸基-3-硫酸酯的糖蛋白或糖脂。这些糖蛋白或糖脂可能被单独靶向,或者可能针对这些表位中的任何组合引发免疫攻击。然而,糖脂,尤其是半乳糖硫酸酯,最近作为非HIV和HIV相关脱髓鞘性神经病潜在免疫事件的介质引起了广泛关注。本综述概述了有或无周围神经功能障碍的HIV感染患者中抗糖脂抗体的最新研究发现,试图就是否这些抗体可能在HIV相关炎症性脱髓鞘性多发性神经病的免疫发病机制中起作用达成一些共识。

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Antibodies in sera from patients with inflammatory demyelinating polyradiculoneuropathy react with ganglioside LM1 and sulphatide of peripheral nerve myelin.炎症性脱髓鞘性多发性神经根神经病患者血清中的抗体与周围神经髓鞘的神经节苷脂LM1和硫脂发生反应。
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Presentation of the same glycolipid by different CD1 molecules.不同CD1分子对同一糖脂的呈递。
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本文引用的文献

1
Studies on the hemolysis of red blood cells by mumps virus. IV. Quantitative study of changes in red blood cell lipides and of virus lipides.腮腺炎病毒对红细胞溶血作用的研究。IV. 红细胞脂质及病毒脂质变化的定量研究。
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Evidence for budding of human immunodeficiency virus type 1 selectively from glycolipid-enriched membrane lipid rafts.1型人类免疫缺陷病毒从富含糖脂的膜脂筏中选择性出芽的证据。
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5
Peripheral nerve binding patterns of anti-sulphatide antibodies in HIV-infected individuals.HIV感染个体中抗硫脂抗体的外周神经结合模式。
Neuroreport. 1999 Jun 3;10(8):1659-64. doi: 10.1097/00001756-199906030-00007.
6
High levels in serum, but no signs of intrathecal synthesis of anti-sulfatide antibodies in HIV-1 infected individuals with or without central nervous system complications.在有或没有中枢神经系统并发症的HIV-1感染个体中,血清中抗硫酸脂抗体水平较高,但无鞘内合成的迹象。
J Neuroimmunol. 1999 Feb 1;94(1-2):153-6. doi: 10.1016/s0165-5728(98)00244-6.
7
Self glycolipids as T-cell autoantigens.自身糖脂作为T细胞自身抗原。
Eur J Immunol. 1999 May;29(5):1667-75. doi: 10.1002/(SICI)1521-4141(199905)29:05<1667::AID-IMMU1667>3.0.CO;2-U.
8
The CD1 system: antigen-presenting molecules for T cell recognition of lipids and glycolipids.CD1系统:用于T细胞识别脂质和糖脂的抗原呈递分子。
Annu Rev Immunol. 1999;17:297-329. doi: 10.1146/annurev.immunol.17.1.297.
9
Antibodies against peripheral myelin glycolipids in people with HIV infection.HIV感染者体内针对外周髓磷脂糖脂的抗体。
Immunol Cell Biol. 1998 Dec;76(6):535-41. doi: 10.1046/j.1440-1711.1998.00778.x.
10
The distribution of CD1 molecules in inflammatory neuropathy.CD1分子在炎性神经病中的分布。
J Neurol Sci. 1998 Jun 30;158(2):154-63. doi: 10.1016/s0022-510x(98)00121-x.