Downregulating galectin-3 inhibits proinflammatory cytokine production by human monocyte-derived dendritic cells via RNA interference

被引：60

作者：

Chen, Swey-Shen ^{[1
,2
,3
]}

Sun, Liang-Wu ^{[1
,2
]}

Brickner, Howard ^{[1
,2
]}

Sun, Pei-Qing ^{[3
]}

机构：

[1] Inst Genet, Dept Immunol, San Diego, CA USA

[2] IGE Therapeut Inc, Dept Allergy Inflammat & Vaccinol, San Diego, CA 92121 USA

[3] Scripps Res Inst, Dept Cell & Mol Biol, La Jolla, CA 92037 USA

来源：

CELLULAR IMMUNOLOGY | 2015年 / 294卷 / 01期

关键词：

Galectin-3; Th17; Dendritic cells; Inflammation; Cytokines; Innate immunity; T-CELLS; INTERLEUKIN; 27; TGF-BETA; ACTIVATION; STIMULATION; EXPRESSION; RECEPTORS; INFECTION; ALLERGEN; ASTHMA;

D O I：

10.1016/j.cellimm.2015.01.017

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Galectin-3 (Gal-3), a B-galactoside-binding lectin, serves as a pattern-recognition receptor (PRR) of dendritic cells (DCs) in regulating proinflammatory cytokine production. Galectin-3 (Gal-3) siRNA downregulates expression of IL-6, IL-1 beta and IL-23 p19, while upregulates IL-10 and IL-12 p35 in TLR/NLR stimulated human MoDCs. Furthermore, Gal-3 siRNA-treated MoDCs enhanced IFN-gamma production in SEB-stimulated CD45RO CD4 T-cells, but attenuated IL-17A and IL-5 production by CD4 T-cells. Addition of neutralizing antibodies against Gal-3, or recombinant Gal-3 did not differentially modulate IL-23 p19 versus IL-12 p35. The data indicate that intracellular Gal-3 acts as cytokine hub of human DCs in responding to innate immunity signals. Gal-3 downregulation reprograms proinflammatory cytokine production by MoDCs that inhibit Th2/Th17 development. (C)2015 Elsevier Inc. All rights reserved.

引用

页码：44 / 53

页数：10