ANTIBODY-RESPONSES TO P(0) AND P(2) MYELIN PROTEINS IN GUILLAIN-BARRE-SYNDROME AND CHRONIC IDIOPATHIC DEMYELINATING POLYRADICULONEUROPATHY

ANTIBODY-RESPONSES TO P(0) AND P(2) MYELIN PROTEINS IN GUILLAIN-BARRE-SYNDROME AND CHRONIC IDIOPATHIC DEMYELINATING POLYRADICULONEUROPATHY
复制标题

DOI:
10.1016/0165-5728(93)90255-w
复制
发表时间:
1993-07-01
影响因子:
3.3
通讯作者:
HUGHES, RAC
HUGHES, RAC
中科院分区:
医学4区
文献类型:
--
作者:
KHALILISHIRAZI, A;ATKINSON, P;HUGHES, RAC

文献摘要

被引文献

相似文献

用外周神经髓鞘蛋白P0或P2免疫诱导动物的炎性神经病变。我们寻求这些蛋白质的抗体与ELISA在38例急性格林-巴利综合征(GBS),32例慢性特发性脱髓鞘性多发性神经根神经病(CIDP),31例其他神经病(ONP)和26例正常对照(NC)受试者。在18.5%的GBS、15.6%的CIDP、6.4%的ONP和3.8%的NC患者血清中发现了抗人P0蛋白IgM抗体。在与P0反应的血清中,来自4/7的GBS、3/5的CIDP、1/2的ONP患者和0/1的NC受试者的血清与合成的P0肽反应,所述合成的P0肽代表来自分子的胞质部分的残基150-169。P0的IgG抗体比IgM抗体稍不常见,仅存在于7.9%的GBS、0%的CIDP和3%的ONP患者以及0%的NC受试者中。我们发现牛P2蛋白抗体比P0抗体更常见。IgM抗体存在于39.5%的GBS、34.4%的CIDP、16.1%的ONP患者和15.4%的NC受试者中。IgG抗体在18.4%的GBS、12.5%的CIDP、3.2%的ONP和7.6%的NC中存在。在含有P2蛋白抗体的血清中,只有少数与P2肽14-25或58-81反应,但没有任何一致的反应模式。我们认为,IgM抗体P0可能有助于脱髓鞘在某些情况下的GBS和CIDP,而更多的。针对P2的常见抗体可能仅仅是同时发生的致病性T细胞介导的应答的标志物。
Immunisation with the peripheral nerve myelin proteins P0 or P2 induces inflammatory neuropathy in animals. We sought antibodies with an ELISA to these proteins in 38 patients with acute Guillain-Barre syndrome (GBS), 32 patients with chronic idiopathic demyelinating polyradiculoneuropathy (CIDP), 31 patients with other neuropathies (ONP) and 26 normal control (NC) subjects. We discovered IgM antibodies to human P0 protein in the sera of 18.5% of the patients with GBS, 15.6% with CIDP, 6.4% with ONP and 3.8% of NC subjects. Of the sera which reacted with P0, sera from 4/7 of GBS, 3/5 of CIDP, 1/2 of ONP patients and 0/1 of NC subjects reacted with a synthetic P0 peptide representing residues 150-169 from the cytoplasmic portion of the molecule. IgG antibodies to P0 were slightly less common than IgM antibodies, being present in only 7.9% of GBS, 0% of CIDP and 3% of ONP patients and 0% of NC subjects. We found antibodies to bovine P2 protein more commonly than antibodies to P0. IgM antibodies were present in 39.5% of GBS, 34.4% of CIDP, 16.1% of ONP patients and 15.4% of NC subjects. IgG antibodies were present in 18.4% of GBS, 12.5% of CIDP, 3.2% of ONP patients and 7.6% of NCs. Of the sera which contained antibodies to P2 protein, only a few reacted with P2 peptides 14-25 or 58-81, but without any consistent pattern of reactivity. We propose that IgM antibodies to P0 may contribute to the demyelination in some cases of GBS and CIDP, whereas the more. common antibodies to P2 may merely be markers of a simultaneous pathogenetic T cell-mediated response.