کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8648531 | 1570696 | 2018 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
HMGB1 regulates T helper 2 and T helper17 cell differentiation both directly and indirectly in asthmatic mice
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کلمات کلیدی
NF-κBp-NF-κBMNCsphorbol 12-myristate 13-acetateRAGEBMDCsBFAHMGB1PBMCsTLRDCsAHRGAPDHAPCscDNA - cDNAComplementary DNA - DNA تکمیلیPMA - LDC هاAsthma - آسمantigen-presenting cells - آنتیژن ارائه سلولinterferon - اینترفرونIFN - اینترفرون هاinterleukin - اینترلوکینBALF - بافتbrefeldin A - برفلدین ADifferentiation - تفکیکTH cells - سلول های THperipheral blood mononuclear cells - سلول های تک هسته ای خون محیطیDendritic cells - سلول های دندریتیکT helper cells - سلول های کمکیMononuclear cells - سلولهای تک هسته ایnuclear factor kappa B - فاکتور هسته ای کاپا BBronchoalveolar lavage fluid - مایع لارو برونکلوفلورAirway hyperresponsiveness - پاسخگویی فوریHigh mobility group box 1 protein - پروتئین جعبه 1 پروتئین گروه تحرکglyceraldehyde 3-phosphate dehydrogenase - گلیسرولیدید 3-فسفات دهیدروژنازToll-like receptors - گیرنده های پولی مانند
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شناسی مولکولی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The Th (T helper) 2 response is characteristic of allergic asthma, and Th17 cells are involved in more severe asthma. Recent studies demonstrated that HMGB1 (High mobility group box 1 protein) regulates airway inflammation and the Th2, Th17 inflammatory response in asthma. HMGB1 can interact with Toll-like receptors (TLR) 2 and 4, and the receptor for advanced glycation end products (RAGE), activating the NF-κB (nuclear factor kappa B) signaling pathway and inducing the release of downstream inflammatory mediators. Both Th cells and dendritic cells express TLR2, TLR4, and RAGE receptors. Therefore, we speculate that HMGB1 could regulate the differentiation of Th2, Th17 cells in asthma through direct and indirect mechanisms. An ovalbumin (OVA)-induced mouse asthmatic model was established. Anti-HMGB1 antibody or rHMGB1 was administered to OVA-sensitized mice 30â¯min prior to each challenge. For in vitro studies, magnetically separated CD4+ naive T cells were stimulated with or without rHMGB1 and/or anti-HMGB1 antibody. BMDCs (bone marrow-derived dendritic cells)-stimulated with or without rHMGB1 and/or anti-HMGB1 antibody were cocultured with CD4+ naive T cells. Our study showed that administration of rHMGB1 aggravated airway inflammation and mucus production, and induced Th2, Th17 polarization in asthmatic mice, and that anti-HMGB1 antibody weakened characteristic features of asthma and blocked the Th2, Th17 inflammatory responses. HMGB1 could directly act on naive T cells to induce differentiation of Th2, Th17 cells in vitro through activating the TLR2, TLR4, RAGE-NF-κB signal pathway in CD4+ naive T cells. HMGB1 could also indirectly promote Th2, Th17 differentiation via activating the TLR2, TLR4, RAGE-NF-κB signal pathway in DCs to mediate their maturation and antigen-presenting ability in vitro.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Immunology - Volume 97, May 2018, Pages 45-55
Journal: Molecular Immunology - Volume 97, May 2018, Pages 45-55
نویسندگان
Ruiting Li, Jing Wang, Fangfang Zhu, Ruifang Li, Bing Liu, Wenjuan Xu, Guangzhen He, Huan Cao, Yimin Wang, Jiong Yang,