Unravelling γδ T-cell dysregulation in the gut and its implications for immune-mediated diseases.

IF 3.3 3区 医学 Q2 CELL BIOLOGY
Disease Models & Mechanisms Pub Date : 2025-09-01 Epub Date: 2025-09-18 DOI:10.1242/dmm.052439
Dilys Santillo, Evangelos Bellos, Vanessa Sancho-Shimizu
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引用次数: 0

Abstract

Multisystem inflammatory syndrome in children (MIS-C) is a rare condition associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and characterised by systemic inflammation and T-cell dysfunction. A subset of patients with MIS-C were found to harbour rare variants in the gene BTNL8 that disrupt BTNL8-BTNL3 heterodimer formation, likely leading to inadequate γδ T-cell regulation and subsequent disrupted gut homeostasis. MIS-C shares clinical features with Kawasaki disease and similar mechanisms of pathogenesis with inflammatory bowel disease, despite these diseases being clinically distinct entities. We explore the common link between these diseases: the potentially critical role gut immunity plays in the initiation and persistence of disease through the tight regulation of γδ T cells via BTNL8 and BTNL3. Understanding the role of BTNL8 in the context of the overlap between these conditions may aid preventative measures and treatment of these conditions.

肠道γδ t细胞失调及其对免疫介导疾病的影响
儿童多系统炎症综合征(MIS-C)是一种与严重急性呼吸综合征冠状病毒2 (SARS-CoV-2)感染相关的罕见疾病,其特征是全身性炎症和t细胞功能障碍。研究发现,一部分患有MIS-C的患者携带罕见的BTNL8基因变异,这种变异会破坏BTNL8- btnl3异源二聚体的形成,可能导致γδ t细胞调节不足,随后破坏肠道内稳态。misc与川崎病具有相同的临床特征,并且与炎症性肠病的发病机制相似,尽管这些疾病在临床上是不同的实体。我们探索了这些疾病之间的共同联系:肠道免疫通过BTNL8和BTNL3对γδ T细胞的严格调节,在疾病的发生和持续中发挥潜在的关键作用。了解BTNL8在这些疾病重叠的背景下的作用可能有助于这些疾病的预防措施和治疗。
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来源期刊
Disease Models & Mechanisms
Disease Models & Mechanisms 医学-病理学
CiteScore
6.60
自引率
7.00%
发文量
203
审稿时长
6-12 weeks
期刊介绍: Disease Models & Mechanisms (DMM) is an online Open Access journal focusing on the use of model systems to better understand, diagnose and treat human disease.
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