自闭症儿童中未发现抗GAD65及其他特异性抗原的抗体。
No Evidence of Antibodies against GAD65 and Other Specific Antigens in Children with Autism.
作者信息
Kalra Simran, Burbelo Peter D, Bayat Ahmad, Ching Kathryn H, Thurm Audrey, Iadarola Michael J, Swedo Susan E
机构信息
Pediatrics and Developmental Branch, National Institutes of Mental Health, National Institutes of Health, Bethesda, MD.
Dental Clinical Research Core, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD.
出版信息
BBA Clin. 2015 Dec 1;4:81-84. doi: 10.1016/j.bbacli.2015.08.001.
BACKGROUND
The presence of autoantibodies has been proposed as evidence for a role of autoimmunity in autism. This report investigates the prevalence of autoantibodies in children with autism using the luciferase immunoprecipitation systems (LIPS) immunoassay technology. A panel of autoantibody targets against several known and candidate neurological autoantigens, autoimmune-associated autoantigens and viruses was employed.
METHODS
Serological analysis was performed on typically developing children (n = 55), developmentally delayed children without autism (n = 24) and children diagnosed with autism (n=104). Autoantibodies were measured against glutamic acid decarboxylase-65 (GAD65), a CNS autoantigen proposed to be associated with autism and against Ro52, glial fibrillary acidic protein, tyrosine hydroxylase, aquaporin-4, and gamma-enolase, the mouse mammary tumor virus and the xenotropic murine leukemia virus. Antibody levels and seropositivity prevalence were analyzed for statistically significant differences between the three groups.
RESULTS
The majority of the children (98%) were seronegative for all targets in the antigen panel. No GAD65 seropositive children were detected in the cohort. Several low level seropositive sera against several of the protein targets were identified in isolated children in each of the three groups, but there was no difference in prevalence.
CONCLUSION
Using this panel of antigens and a sensitive, robust assay, no evidence of unusual immunoreactivity was detected in children with autism, providing evidence against a role of autoimmunity against several previously implicated proteins in autism spectrum disorder pathogenesis.
GENERAL SIGNIFICANCE
The idea that autoantibodies represent an underlying cause or are biomarkers for autism pathophysiology is not supported by this report.
背景
自身抗体的存在被认为是自身免疫在自闭症中起作用的证据。本报告使用荧光素酶免疫沉淀系统（LIPS）免疫测定技术调查自闭症儿童中自身抗体的流行情况。采用了一组针对几种已知和候选神经自身抗原、自身免疫相关自身抗原和病毒的自身抗体靶点。
方法
对发育正常的儿童（n = 55）、无自闭症的发育迟缓儿童（n = 24）和被诊断为自闭症的儿童（n = 104）进行血清学分析。检测针对谷氨酸脱羧酶-65（GAD65，一种被认为与自闭症相关的中枢神经系统自身抗原）、Ro52、胶质纤维酸性蛋白、酪氨酸羟化酶、水通道蛋白-4、γ-烯醇化酶、小鼠乳腺肿瘤病毒和嗜异性小鼠白血病病毒的自身抗体。分析三组之间抗体水平和血清阳性率的统计学显著差异。
结果
大多数儿童（98%）对抗原组中的所有靶点血清学阴性。该队列中未检测到GAD65血清阳性儿童。在三组中的个别儿童中均鉴定出针对几种蛋白质靶点的低水平血清阳性，但流行率无差异。
结论
使用该抗原组和灵敏、可靠的检测方法，未在自闭症儿童中检测到异常免疫反应的证据，这为反对自身免疫在自闭症谱系障碍发病机制中对几种先前涉及的蛋白质起作用提供了证据。
一般意义
本报告不支持自身抗体是自闭症病理生理学的潜在原因或生物标志物这一观点。
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