T cell populations in children with autism spectrum disorder and co-morbid gastrointestinal symptoms.
T cell populations in children with autism spectrum disorder and co-morbid gastrointestinal symptoms.
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DOI：
10.1016/j.bbih.2020.100042
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发表时间：
2020-02
期刊：
影响因子：
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通讯作者：
D. Rose;Houa Yang;M. Careaga;K. Angkustsiri;J. Van de Water;P. Ashwood
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文献类型：
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作者：
D. Rose;Houa Yang;M. Careaga;K. Angkustsiri;J. Van de Water;P. Ashwood
患有ASD的儿童比典型发育的儿童更容易出现胃肠道（GI）症状。许多研究报告了大多数自闭症谱系障碍患者的免疫异常和炎症特征。免疫功能障碍通常被假设为许多胃肠道疾病的驱动因素，并且已经表明，它在表现出胃肠道症状的ASD儿童中更明显。在这项研究中，我们试图描述有和没有GI症状的儿童与健康的典型发育儿童相比，外周血T细胞亚群的特征。从参与者中分离出外周血单核细胞，他们被分为三组：患有ASD的儿童经历GI症状（n = 14），患有ASD的儿童没有经历GI症状（n = 10）和典型发育的儿童没有经历GI症状（n = 15）。为了被纳入GI组，GI症状，如腹泻，便秘和/或排便时疼痛，必须在过去6个月内定期出现在儿童中;同样，为了被纳入无GI组，排便不能包括在整个发育过程中出现的上述症状。评估细胞的表面标志物和细胞内细胞因子以鉴定T细胞群。有ASD和GI症状的儿童显示出升高的TH 17群体（0.757% ± 0.313%对比0.297% ± 0.197），而没有经历GI症状的ASD儿童显示出升高的TH 2群体频率（2.02% ± 1.08%对比1.01% ± 0.58%）。与正常发育的儿童相比，两个ASD组均显示出肠道归巢调节性T细胞群减少的证据（ASDGI：1.93% ± 0.75%和ASDNoGI：1.85% ± 0.89，相比之下为2.93% ± 1.16%）。ASD儿童可能存在免疫调节缺陷，导致不同的炎性T细胞亚群，这些亚群可能与相关的合并症有关。
Children with ASD are more likely to experience gastrointestinal (GI) symptoms than typically-developed children. Numerous studies have reported immune abnormalities and inflammatory profiles in the majority of individuals with ASD. Immune dysfunction is often hypothesized as a driving factor in many GI diseases and it has been suggested that it is more apparent in children with ASD that exhibit GI symptoms. In this study we sought to characterize peripheral T cell subsets in children with and without GI symptoms, compared to healthy typically-developing children. Peripheral blood mononuclear cells were isolated from participants, who were categorized into three groups: children with ASD who experience GI symptoms (n = 14), children with ASD who do not experience GI symptoms (n = 10) and typically-developing children who do not experience GI symptoms (n = 15). In order to be included in the GI group, GI symptoms such as diarrhea, constipation, and/or pain while defecating, had to be present in the child regularly for the past 6 months; likewise, in order to be placed in the no GI groups, bowel movements could not include the above symptoms present throughout development. Cells were assessed for surface markers and intracellular cytokines to identify T cell populations. Children with ASD and GI symptoms displayed elevated TH17 populations (0.757% ± 0.313% compared to 0.297% ± 0.197), while children with ASD who did not experience GI symptoms showed increased frequency of TH2 populations (2.02% ± 1.08% compared to 1.01% ± 0.58%). Both ASD groups showed evidence of reduced gut homing regulatory T cell populations compared to typically developing children (ASDGI:1.93% ± 0.75% and ASDNoGI:1.85% ± 0.89 compared to 2.93% ± 1.16%). Children with ASD may have deficits in immune regulation that lead to differential inflammatory T cell subsets that could be linked to associated co-morbidities.