Differential Roles of Dendritic Cells in Expanding CD4 T Cells in Sepsis

Persistent ID (NDL): info:ndljp/pid/11671779

Material type: 博士論文

Author: Darkwah, Samuel

Publisher: 三重大学

Publication date: 2020-09-16

Material Format: Digital

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Name of awarding university/degree: 三重大学,博士(医学)

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Note (General)：: application/pdfSepsis is a systemically dysregulated inflammatory syndrome, in which dendritic cells (DCs) play a critical role in coordinating aberra...

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Material Type: 博士論文
Title: Differential Roles of Dendritic Cells in Expanding CD4 T Cells in Sepsis
Author/Editor: Darkwah, Samuel
Author Heading: Darkwah, Samuel
Publication, Distribution, etc.: 三重大学
Publication Date: 2020-09-16
Publication Date (W3CDTF): 2020-09-16
Degree grantor/type: 三重大学
Date Granted: 2020-09-16
Date Granted (W3CDTF): 2020-09-16
Dissertation Number: 甲医学第2032号
Degree Type: 博士(医学)
Conferring No. (Dissertation): 甲医学第2032号
Text Language Code: eng
Subject Heading: sepsis
spleen
mesenteric lymph nodes
dendritic cells
CD4 T cells
IL-1β
Target Audience: 一般
Note (General): application/pdf
Sepsis is a systemically dysregulated inflammatory syndrome, in which dendritic cells (DCs) play a critical role in coordinating aberrant immunity. The aim of this study is to shed light on the differential roles played by systemic versus mucosal DCs in regulating immune responses in sepsis. We identified a differential impact of the systemic and mucosal DCs on proliferating allogenic CD4 T cells in a mouse model of sepsis. Despite the fact that the frequency of CD4 T cells was reduced in septic mice, septic mesenteric lymph node (MLN) DCs proved superior to septic spleen (SP) DCs in expanding allogeneic CD4 T cells. Moreover, septic MLN DCs markedly augmented the surface expression of MHC class II and CD40, as well as the messaging of interleukin-1β(IL-1β). Interestingly, IL-1β-treated CD4 T cells expanded in a dose-dependent manner, suggesting that this cytokine acts as a key mediator of MLN DCs in promoting septic inflammation. Thus, mucosal and systemic DCs were found to be functionally different in the way CD4 T cells respond during sepsis. Our study provides a molecular basis for DC activity, which can be differential in nature depending on location, whereby it induces septic inflammation or immune-paralysis.
本文/Department of Molecular Pathobiology and Cell Adhesion Biology, Mie University Graduate School of Medicine, Tsu, Mie 514-8507, Japan
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DOI: info:doi/10.3390/biomedicines7030052
https://doi.org/info:doi/10.3390/biomedicines7030052
Persistent ID (NDL): info:ndljp/pid/11671779
https://dl.ndl.go.jp/pid/11671779
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Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文
https://dl.ndl.go.jp/collections/A00014
Acquisition Basis: 博士論文（自動収集）
Date Accepted (W3CDTF): 2021-05-16T23:51:55+09:00
Date Created (W3CDTF): 2021-01-05
Format (IMT): application/pdf
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Periodical Title (URI): http://hdl.handle.net/10076/00019576
https://mie-u.repo.nii.ac.jp/records/13958
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