Please use this identifier to cite or link to this item: http://scholarbank.nus.edu.sg/handle/10635/17539
Title: Investigation of Interleukin 1B synthesis and secretion by dendritic cells: Interplay between toll-like receptor and FCG receptor
Authors: WU XIAOWEI
Keywords: Interleukin 1B; dendritic cells; Fc gamma receptor; P2X7 receptor;
Issue Date: 12-Apr-2007
Source: WU XIAOWEI (2007-04-12). Investigation of Interleukin 1B synthesis and secretion by dendritic cells: Interplay between toll-like receptor and FCG receptor. ScholarBank@NUS Repository.
Abstract: Interleukin-1I? (IL-1I?) is a prototypic multifunctional cytokine. It not only mediates inflammatory response in innate immunity, but also modulates antigen-specific immunity. Dendritic cells (DCs) are central regulator of immune activation and tolerance. However, the regulation of IL-1I? production in DCs is less clear. In this project, the underlying regulatory mechanisms of IL-1I? synthesis and secretion in monocyte-derived DCs (moDCs) are investigated. It was observed that, LPS stimulation induced moDCs to express IL-1I? mRNA, synthesize pro-IL-1I? and process IL-1I?i? precursors, but with little mature IL-1I? secretion; immobilized IgG (imIgG) stimulation induced little IL-1I? mRNA expression and protein synthesis by moDCs. However, co-stimulation with LPS and imIgG resulted in dramatic increase in IL-1I? secretion from moDCs. The increase was mediated through P2X7 receptor-dependent Ca2+ influx. In addition, Rac1, JNK and MEK were identified as key molecules in LPS/imIgG-induced IL-1I? production and secretion by moDCs, whilst PI3-K and p38 MAPK as negative modulators.
URI: http://scholarbank.nus.edu.sg/handle/10635/17539
Appears in Collections:Master's Theses (Open)

Show full item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
Thesis-Wu Xiaowei.pdf2.02 MBAdobe PDF

OPEN

NoneView/Download

Page view(s)

192
checked on Jan 22, 2018

Download(s)

194
checked on Jan 22, 2018

Google ScholarTM

Check


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.