无麸质饮食对乳糜泻患者外周血中 HLA-DQ2 和 TRAFD1 基因表达的影响

IF 4.7 Q2 IMMUNOLOGY Journal of Translational Autoimmunity Pub Date : 2024-04-09 DOI:10.1016/j.jtauto.2024.100240
Mariavittoria Laezza , Laura Pisapia , Benedetta Toro , Vincenzo Mercadante , Antonio Rispo , Carmen Gianfrani , Giovanna Del Pozzo
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引用次数: 0

摘要

背景乳糜泻(CD)是一种慢性免疫介导的肠病,由饮食中的麸质引起,易感基因携带编码 DQ2.5 和 DQ8 分子的 HLA(人类白细胞抗原)基因。TRAFD1(TRAF 型锌指结构域 1)是最近发现的一种与 CD 相关的基因,被定义为 IFNγ 信号和 MHC I 类抗原处理/呈递的主调节器。目前尚无特效药物治疗,唯一有效的治疗方法是无麸质饮食(GFD)。绝大多数乳糜泻患者在接受无麸质饮食后,症状会完全缓解,肠道粘膜结构和功能也会恢复。到目前为止,很少有研究调查 CD 患者在接受 GFD 治疗后的分子差异。方法我们观察了急性 CD 成人患者在接受 GFD 治疗时和接受治疗后 HLA DQ2.5 和 TRAFD1 风险基因的表达情况。结果当我们比较 HLA-DQ mRNA 的表达时,我们没有发现两组患者之间有明显的差异,这表明 GFD 患者与活动性疾病患者一样有能力向同源 T 细胞展示麦胶蛋白抗原。相反,TRAFD1 在接受治疗的 CD 患者的 PBMC 中表达较多。值得注意的是,在纵向分析的 GFD 患者中,TRAFD1 转录物显著增加,表明其在下调麸质诱导的炎症通路中发挥作用。
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Changes upon the gluten-free diet of HLA-DQ2 and TRAFD1 gene expression in peripheral blood of celiac disease patients

Background

Celiac disease (CD) is a chronic immuno-mediated enteropathy caused by dietary gluten in genetically susceptible individuals carrying HLA (Human Leukocytes Antigen) genes that encode for DQ2.5 and DQ8 molecules. TRAFD1 (TRAF-type zinc finger domain 1) is a gene recently found associated with CD and defined as a master regulator of IFNγ signalling and of MHC class I antigen processing/presentation. There is no specific drug therapy and the only effective treatment is the gluten-free diet (GFD). The great majority of celiac patients when compliant with GFD have a complete remission of symptoms and recovery of gut mucosa architecture and function. Until now, very few studies have investigated molecular differences occurring in CD patients upon the GFD therapy.

Methods

We looked at the expression of both HLA DQ2.5 and TRAFD1 risk genes in adult patients with acute CD at the time of and in treated patients on GFD. Specifically, we measured by qPCR the HLA-DQ2.5 and TRAFD1 mRNAs on peripheral blood mononuclear cells (PBMC) from the two groups of patients.

Results

When we compared the HLA-DQ mRNA expression, we didn't find significant variation between the two groups of patients, thus indicating that GFD patients have the same capability to present gliadin antigens to cognate T cells as patients with active disease. Conversely, TRAFD1 was more expressed in PBMC from treated CD subjects. Notably, TRAFD1 transcripts significantly increased in the patients analyzed longitudinally during the GFD, indicating a role in the downregulation of gluten-induced inflammatory pathways.

Conclusion

Our study demonstrated that HLA-DQ2.5 and TRAFD1 molecules are two important mediators of anti-gluten immune response and inflammatory process.

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来源期刊
Journal of Translational Autoimmunity
Journal of Translational Autoimmunity Medicine-Immunology and Allergy
CiteScore
7.80
自引率
2.60%
发文量
33
审稿时长
55 days
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