[1] PubMed ID: | 35122570 |
Disease Name: | Rhinitis, Allergic |
Sample: | PBMCs, CD4+ T cells, Tregs, and nasal tissues of AR patients |
Dysfunction Pattern: | Interaction(miR-16/ATXN2L axis) |
Validated Method: | Western Blot//Transection//qRT-PCR//Flow Cytometry//CCK8//Luciferase Report Assay//ELISA |
Description: | lncRNA HCP5 expression dramatically downregulated in PBMCs, CD4+ T cells, Tregs, and nasal tissues of AR patients, as well as in IL-13-treated NECs.HCP5 promoted Tregs differentiation and proliferation via targeting miR-16/ATXN2L axis. Additionally, HCP5 inhibited IL-13-induced GM-CSF, eotaxin, and MUC5AC production in NECs. HCP5 sponged miR-16 and negatively regulated its expression, and miR-16 targeted ATXN2L and inhibition of miR-16 suppressed IL-13-induced GM-CSF, eotaxin, and MUC5AC expression. HCP5/miR-16/ATXN2L axis mediated Tregs proliferation and functions in AR. Besides, the regulation of IL-13-induced dysfunction of NECs by lncRNA HCP5 depended on miR-16/ATXN2L in the inflammatory response of AR. |
Causality: | Yes |
Causal Description: | HCP5 promoted Tregs differentiation and proliferation via targeting miR-16/ATXN2L axis. |
Clinical-realted Application: | |
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