کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6116697 | 1216379 | 2014 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
p38 Mitogen-Activated Protein Kinase in beryllium-induced dendritic cell activation
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
NF-κBLPSPBMCsJnkBESCBDAPCsTLRiDCsDCsmoDCsp38MAPKMonocyte-derived DC - DC مونوسیت مشتق شدهERKs - ERK هاMAPK - MAPKAntigen presenting cells - آنتیژن ارائه سلولRIPA buffer - بافر RIPAradioimmunoprecipitation buffer - بافر رادیویمونوپراکسیدberyllium - بریلیوم Chronic Beryllium Disease - بیماری بریلیم مزمنLymphocyte proliferation - تکثیر لنفوسیتToll-like receptor - تیالآرperipheral blood mononuclear cells - سلول های تک هسته ای خون محیطیDendritic cells - سلول های دندریتیکimmature dendritic cells - سلولهای دندریتیک نابالغlipopolysaccharide - لیپوپلی ساکاریدmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenExtracellular regulated kinases - کیناز تنظیم شده خارج سلولی
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Dendritic cells (DC) play a role in the regulation of immune responses to haptens, which in turn impact DC maturation. Whether beryllium (Be) is able to induce DC maturation and if this occurs via the MAPK pathway is not known. Primary monocyte-derived DCs (moDCs) models were generated from Be non-exposed healthy volunteers as a non-sensitized cell model, while PBMCs from BeS (Be sensitized) and CBD (chronic beryllium disease) were used as disease models. The response of these cells to Be was evaluated. The expression of CD40 was increased significantly (p < 0.05) on HLA-DP Glu69+ moDCs after 100 μM BeSO4-stimulation. BeSO4 induced p38MAPK phosphorylation, while IκB-α was degraded in Be-stimulated moDCs. The p38 MAPK inhibitor SB203580 blocked Be-induced NF-κB activation in moDCs, suggesting that p38MAPK and NF-κB are dependently activated by BeSO4. Furthermore, in BeS and CBD subjects, SB203580 downregulated Be-stimulated proliferation in a dose-dependent manner, and decreased Be-stimulated TNF-α and IFNγ cytokine production. Taken together, this study suggests that Be-induces non-sensitized Glu69+ DCs maturation, and that p38MAPK signaling is important in the Be-stimulated DCs activation as well as subsequent T cell proliferation and cytokine production in BeS and CBD. In total, the MAPK pathway may serve as a potential therapeutic target for human granulomatous lung diseases.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Human Immunology - Volume 75, Issue 12, December 2014, Pages 1155-1162
Journal: Human Immunology - Volume 75, Issue 12, December 2014, Pages 1155-1162
نویسندگان
L. Li, Z. Huang, M. Gillespie, P.M. Mroz, L.A. Maier,