Repository logo
  • English
  • 中文
Log In
Have you forgotten your password?
  1. Home
  2. College of Medicine / 醫學院
  3. Immunology / 免疫學研究所
  4. Effects of Inflammatory Response on Dendritic Cell Development from CLPs
 
  • Details

Effects of Inflammatory Response on Dendritic Cell Development from CLPs

Date Issued
2014
Date
2014
Author(s)
Chao, Ying-Yin
URI
http://ntur.lib.ntu.edu.tw//handle/246246/262032
Abstract
Toll-like receptors (TLRs) are one family of the pattern recognition receptors in the innate immunity to sense and response to microbial or viral infection. TLRs are expressed in innate immune cells, including macrophage and dendritic cells (DC) and non-immune cells such as epithelium in the gut and lung. Interestingly, TLRs also expressed in hematopoietic stem and progenitor cells (HSPCs). However, the roles of TLR response in HSPCs are largely unknown. We showed here that Flt3 ligand (FL) preferentially promoted pDC formation from common lymphoid progenitor (CLP), while TLR9 signaling promoted cDC differentiation. CpG ODN alone or CpG ODN plus FL, and not FL alone, also induced an unique DC population, which expressed both CD11b and B220 (double positive) other than CD11c. Interestingly, the morphology and phenotype of these DPDCs were more closer to those of cDCs and not to those of pDCs. The development of CpG-induced cDCs and DPDCs were not altered in the absence of STAT1, or IFNAR1, the type I interferon (IFN-I) receptor, suggesting that the process is IFN-I-independent. However, the effect of CpG ODN on DC development was dependent on direct TLR9 signaling pathway and not on TLR9-induced genes, as biased cDC development was impaired in Tlr9-/- CLPs when co-cultured with WT CLPs. Moreover, this effect was abolished in the absence of STAT3, suggesting that STAT3 might positively regulate TLR9-induced development of cDC and DPDC. These results suggest that inflammation-induced remodeling of DC population may provide a unique way for a rapid reaction of the innate immune system upon infection or inflammation.
Subjects
樹突細胞發育
發炎反應
淋巴共同前驅細胞
類鐸受體
活化訊號傳導與轉錄子三
Type
thesis
File(s)
Loading...
Thumbnail Image
Name

ntu-103-R01449011-1.pdf

Size

23.32 KB

Format

Adobe PDF

Checksum

(MD5):56fdf5a1ad7416044a6e36e944c809a5

臺大位居世界頂尖大學之列,為永久珍藏及向國際展現本校豐碩的研究成果及學術能量,圖書館整合機構典藏(NTUR)與學術庫(AH)不同功能平台,成為臺大學術典藏NTU scholars。期能整合研究能量、促進交流合作、保存學術產出、推廣研究成果。

To permanently archive and promote researcher profiles and scholarly works, Library integrates the services of “NTU Repository” with “Academic Hub” to form NTU Scholars.

總館學科館員 (Main Library)
醫學圖書館學科館員 (Medical Library)
社會科學院辜振甫紀念圖書館學科館員 (Social Sciences Library)

開放取用是從使用者角度提升資訊取用性的社會運動,應用在學術研究上是透過將研究著作公開供使用者自由取閱,以促進學術傳播及因應期刊訂購費用逐年攀升。同時可加速研究發展、提升研究影響力,NTU Scholars即為本校的開放取用典藏(OA Archive)平台。(點選深入了解OA)

  • 請確認所上傳的全文是原創的內容,若該文件包含部分內容的版權非匯入者所有,或由第三方贊助與合作完成,請確認該版權所有者及第三方同意提供此授權。
    Please represent that the submission is your original work, and that you have the right to grant the rights to upload.
  • 若欲上傳已出版的全文電子檔,可使用Open policy finder網站查詢,以確認出版單位之版權政策。
    Please use Open policy finder to find a summary of permissions that are normally given as part of each publisher's copyright transfer agreement.
  • 網站簡介 (Quickstart Guide)
  • 使用手冊 (Instruction Manual)
  • 線上預約服務 (Booking Service)
  • 方案一:臺灣大學計算機中心帳號登入
    (With C&INC Email Account)
  • 方案二:ORCID帳號登入 (With ORCID)
  • 方案一:定期更新ORCID者,以ID匯入 (Search for identifier (ORCID))
  • 方案二:自行建檔 (Default mode Submission)
  • 方案三:學科館員協助匯入 (Email worklist to subject librarians)

Built with DSpace-CRIS software - Extension maintained and optimized by 4Science