A Chinese Patent Medicine JiaYanKangTai Alleviates Inflammatory Lesions of Experimental Autoimmune Thyroiditis by Regulating Interleukin-17 Signaling

Pan, Yajing; Zhang, Qiue; Zhang, Chengfei; Wu, Li; Qin, Lingling; Liu, Tonghua; Hu, Kaiwen

doi:10.3389/fendo.2021.794568

Cited by 2 publications

(1 citation statement)

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“…In addition, the down-regulation of RAC1 was linked with ERK1/2 pathways which favor the protection of thyrocyte cells [ 38 ] and other cell types [ 23 ] from inflammation-induced apoptosis. A recent study demonstrated that a Chinese patent medicine decreased both levels of TgAb and TPOAb, and alleviated lymphocytic infiltration by regulating expressions of p-ERK1/2 in a rat model [ 39 ], which further highlighted the crucial role of ERK1/2 signals in the HT progression.…”

Section: Discussionmentioning

confidence: 99%

miR-142-3p encapsulated in T lymphocyte-derived tissue small extracellular vesicles induces Treg function defect and thyrocyte destruction in Hashimoto’s thyroiditis

Huang

et al. 2023

BMC Med

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Background Hashimoto’s thyroiditis (HT) is an organ-specific autoimmune disease characterized by lymphocyte infiltration that destroys thyrocyte cells. The aim of the present study was to elucidate the role and mechanisms of tissue small extracellular vesicle (sEV) microRNAs (miRNAs) in the pathogenesis of HT. Methods Differentially expressed tissue sEV miRNAs were identified between HT tissue and normal tissue by RNA sequencing in the testing set (n = 20). Subsequently, using quantitative real-time polymerase chain reaction (qRT‒PCR) assays and logistic regression analysis in the validation set (n = 60), the most relevant tissue sEV miRNAs to HT were verified. The parental and recipient cells of that tissue sEV miRNA were then explored. In vitro and in vivo experiments were further performed to elucidate the function and potential mechanisms of sEV miRNAs that contribute to the development of HT. Results We identified that miR-142-3p encapsulated in T lymphocyte-derived tissue sEVs can induce Treg function defect and thyrocyte destruction through an intact response loop. Inactivation of miR-142-3p can effectively protect non-obese diabetic (NOD).H-2h4 mice from HT development display reduced lymphocyte infiltration, lower antibody titers, and higher Treg cells. Looking at the mechanisms underlying sEV action on thyrocyte destruction, we found that the strong deleterious effect mediated by tissue sEV miR-142-3p is due to its ability to block the activation of the ERK1/2 signaling pathway by downregulating RAC1. Conclusions Our findings highlight the fact that tissue sEV-mediated miR-142-3p transfer can serve as a communication mode between T lymphocytes and thyrocyte cells in HT, favoring the progression of HT.

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Section: Discussionmentioning

confidence: 99%