Rose Destanie R, Yang Houa, Careaga Milo, Angkustsiri Kathy, Van de Water Judy, Ashwood Paul
Department of Medical Microbiology and Immunology, University of California Davis, Davis, CA, USA.
MIND Institute, University of California Davis, Davis, CA, USA.
Brain Behav Immun Health. 2020 Jan 26;2:100042. doi: 10.1016/j.bbih.2020.100042. eCollection 2020 Feb.
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 T17 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 T2 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 (ASD:1.93% ± 0.75% and ASD: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.
与发育正常的儿童相比,患有自闭症谱系障碍(ASD)的儿童更易出现胃肠道(GI)症状。大量研究报告称,大多数ASD患者存在免疫异常和炎症特征。免疫功能障碍常被认为是许多胃肠道疾病的驱动因素,有人提出,在出现GI症状的ASD儿童中,这种情况更为明显。在本研究中,我们试图对有和没有GI症状的ASD儿童的外周血T细胞亚群进行特征分析,并与发育正常的健康儿童进行比较。从参与者中分离出外周血单核细胞,这些参与者被分为三组:有GI症状的ASD儿童(n = 14)、无GI症状的ASD儿童(n = 10)和无GI症状的发育正常儿童(n = 15)。为了纳入GI组,过去6个月内儿童必须经常出现腹泻、便秘和/或排便时疼痛等GI症状;同样,为了纳入无GI组,整个发育过程中排便不能出现上述症状。对细胞进行表面标志物和细胞内细胞因子评估,以识别T细胞群体。有ASD和GI症状的儿童显示T17群体升高(分别为0.757%±0.313%和0.297%±0.197%),而无GI症状的ASD儿童显示T2群体频率增加(分别为2.02%±1.08%和1.01%±0.58%)。与发育正常的儿童相比,两个ASD组均显示肠道归巢调节性T细胞群体减少(ASD组分别为1.93%±0.75%和1.85%±0.89%,发育正常儿童为2.93%±1.16%)。患有ASD的儿童可能存在免疫调节缺陷,导致不同的炎症性T细胞亚群,这可能与相关的合并症有关。