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Dysregulation of non-coding RNAs in autoimmune thyroid disease
被引:12
|作者:
Taheri, Mohammad
[1
]
Eghtedarian, Reyhane
[2
]
Dinger, Marcel E.
[3
]
Ghafouri-Fard, Soudeh
[2
]
机构:
[1] Shahid Beheshti Univ Med Sci, Urogenital Stem Cell Res Ctr, Tehran, Iran
[2] Shahid Beheshti Univ Med Sci, Dept Med Genet, Tehran, Iran
[3] Univ New South Wales, Sch Biotechnol & Biomol Sci, Sydney, NSW, Australia
关键词:
Autoimmune thyroid disease;
AITD;
Hashimoto's thyroiditis;
Graves' disease;
miRNA;
lncRNA;
CTLA-4 GENE POLYMORPHISM;
BLOOD MONONUCLEAR-CELLS;
GRAVES-DISEASE;
MICRORNA EXPRESSION;
SUSCEPTIBILITY;
ASSOCIATIONS;
PREVALENCE;
TRANSCRIPT;
GENERATION;
RECEPTOR;
D O I:
10.1016/j.yexmp.2020.104527
中图分类号:
R36 [病理学];
学科分类号:
100104 ;
摘要:
Autoimmune thyroid disease (AITD) is a complex disorder with both genetic and environmental risk factors. A number of genetic factors such as HLA and CTLA-4 loci have been associated with risk of this disorder. In addition to these factors, recent studies have shown contribution of non-coding RNAs in the pathogenesis of this condition. Several microRNAs (miRNAs) and a number of long noncoding RNAs (lncRNAs) such as IFNG-AS1, Heg, NR_038461, NR_038462, T204821 and NR_104125 have been dysregulated in peripheral blood of patients with AITD. These transcripts are mostly enriched in pathways that modulate humoral and cellular immune responses such as those associated with antigen presentation and differentiation of Th1, Th2 and Th17 cells. Functional studies verified the role of a number of lncRNAs and miRNAs in regulation of critical immune-related pathways in AITD. Thus, they participate in the pathophysiology of AITD. In the current review, we summarize the results of studies that assessed participation of non-coding RNAs in the pathophysiology of AITD.
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页数:10
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