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Antibodies prepared to neuronal glutamate receptor subunit3 bind IFNalpha-receptors: implications for an autoimmune process.

作者信息

Gahring L C, Carlson N G, Rogers S W

机构信息

Salt Lake City Veteran's Administration Geriatrics Research, Education and Clinical Center (GRECC) and University of Utah School of Medicine, Salt Lake City 84112, USA.

出版信息

Autoimmunity. 1998;28(4):243-8. doi: 10.3109/08916939808995372.

DOI:10.3109/08916939808995372
PMID:9892506
Abstract

Anti-glutamate receptor (GluR) agonist-like antibodies prepared in rabbits that are similar to autoantibodies found in Rasmussen's encephalitis (RE) were found to exhibit greater immunoreactivity towards human interferon alpha receptor (IFNAR-1) than to GluR3. Since antibodies prepared to a defined region of GluR3 can react preferentially to an unrelated sequence in the human IFNAR-1, we propose that the IFNAR-1 may be an heteroclitic antigen of GluR3. These results suggest that differential reactivity toward heteroclitic antigens may contribute to variable clinical characteristics of certain autoimmune diseases.

摘要

相似文献

1
Antibodies prepared to neuronal glutamate receptor subunit3 bind IFNalpha-receptors: implications for an autoimmune process.
Autoimmunity. 1998;28(4):243-8. doi: 10.3109/08916939808995372.
2
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Autoantibodies to glutamate receptors can damage the brain in epilepsy, systemic lupus erythematosus and encephalitis.针对谷氨酸受体的自身抗体可在癫痫、系统性红斑狼疮和脑炎中损害大脑。
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引用本文的文献

1
Glutamate receptor antibodies in neurological diseases: anti-AMPA-GluR3 antibodies, anti-NMDA-NR1 antibodies, anti-NMDA-NR2A/B antibodies, anti-mGluR1 antibodies or anti-mGluR5 antibodies are present in subpopulations of patients with either: epilepsy, encephalitis, cerebellar ataxia, systemic lupus erythematosus (SLE) and neuropsychiatric SLE, Sjogren's syndrome, schizophrenia, mania or stroke. These autoimmune anti-glutamate receptor antibodies can bind neurons in few brain regions, activate glutamate receptors, decrease glutamate receptor's expression, impair glutamate-induced signaling and function, activate blood brain barrier endothelial cells, kill neurons, damage the brain, induce behavioral/psychiatric/cognitive abnormalities and ataxia in animal models, and can be removed or silenced in some patients by immunotherapy.神经疾病中的谷氨酸受体抗体：抗AMPA - GluR3抗体、抗NMDA - NR1抗体、抗NMDA - NR2A/B抗体、抗mGluR1抗体或抗mGluR5抗体存在于以下疾病患者的亚组中：癫痫、脑炎、小脑共济失调、系统性红斑狼疮（SLE）和神经精神性SLE、干燥综合征、精神分裂症、躁狂症或中风。这些自身免疫性抗谷氨酸受体抗体可在少数脑区与神经元结合，激活谷氨酸受体，降低谷氨酸受体的表达，损害谷氨酸诱导的信号传导和功能，激活血脑屏障内皮细胞，杀死神经元，损伤大脑，在动物模型中诱发行为/精神/认知异常和共济失调，并且在一些患者中可通过免疫疗法去除或使其失活。
J Neural Transm (Vienna). 2014 Aug;121(8):1029-75. doi: 10.1007/s00702-014-1193-3. Epub 2014 Aug 1.
2
Pharmacology of AMPA/kainate receptor ligands and their therapeutic potential in neurological and psychiatric disorders.AMPA/红藻氨酸受体配体的药理学及其在神经和精神疾病中的治疗潜力。
Drugs. 2000 Jan;59(1):33-78. doi: 10.2165/00003495-200059010-00004.