%0 Journal Article
%T Apolipoprotein A-I inhibited group II innate lymphoid cell response mediated by microRNA-155 in allergic rhinitis.
%A Zeng Y
%A Zeng Q
%A Wen Y
%A Li J
%A Xiao H
%A Yang C
%A Luo R
%A Liu W
%J J Allergy Clin Immunol Glob
%V 3
%N 2
%D 2024 May
%M 38371899
暂无%R 10.1016/j.jacig.2024.100212
%X <B>UNASSIGNED: </B>Group 2 innate lymphoid cells (ILC2s) have been found to take part in type 2 inflammation by secreting TH2 cytokines. Apolipoprotein A-I (Apo-AI), a major structural and functional protein of high-density lipoproteins, has anti-inflammatory effects on neutrophils, monocytes, macrophages, and eosinophils. However, its effects on ILC2s are not well characterized.<BR><B>UNASSIGNED: </B>We aimed to investigate the effect of Apo-AI on the proliferation and function of ILC2s as well as its possible mechanism.<BR><B>UNASSIGNED: </B>The protein expression of Apo-AI and the percentage of ILC2s in peripheral blood between 20 allergic rhinitis patients and 20 controls were detected by ELISA and flow cytometry. The effect of Apo-AI and miR-155 on ILC2 proliferation and function was detected by tritiated thymidine incorporation and ELISA. Anima models were adopted to verify the effect of Apo-AI in vivo.<BR><B>UNASSIGNED: </B>Elevated expression of Apo-AI was observed in allergic rhinitis patients. Apo-AI promotes ABCA1 expression by ILC2s, which can be inhibited by anti-Apo-AI. Apo-AI decreased ILC2 proliferation and the microRNA levels of GATA3 and RORα from ILC2s. The miR-155 overexpression promoted the upregulation of GATA3 and type II cytokines from ILC2s, while the addition of Apo-AI or miR-155 inhibitor significantly inhibited expression of GATA3 and type II cytokines by ILC2s. Apo-AI-/- mice showed as enhanced allergen-induced airway inflammation. The miR-155 inhibitor can reverse the enhanced allergen-induced airway inflammation in Apo-AI-/- mice, while miR-155 mimics can reverse the decreased allergen-induced airway inflammation in Apo-AI-treated mice.<BR><B>UNASSIGNED: </B>Apo-AI suppressed the proliferation and function of ILC2s through miR-155 in allergic rhinitis. Our data provide new insights into the mechanism of allergen-induced airway inflammation.