2012 Fiscal Year Final Research Report
Molecular analysis of pathogenesis on rheumatoid arthritis caused by chemokines CCL19 and CCL21
Project/Area Number |
22790945
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Single-year Grants |
Research Field |
膠原病・アレルギー・感染症内科学
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Research Institution | Toho University |
Principal Investigator |
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Project Period (FY) |
2010 – 2012
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Keywords | 臨床免疫学 |
Research Abstract |
The roles for chemokines CCL19 and CCL21 in induction of collagen-induced arthritis (CIA) were investigated plt mutant mice, that lacking expression of CCL19 and CCL21. We found that these mutant mice failed to express inflammatory cytokines and showed resistant to the induction of CIA. Collagen-immunized plt mice decreased IL-23 production in dendritic cells and a concomitant defect in Th17 cells. CCL19- and CCL21-mediated activation of the PI3K/Akt pathway and NF-κB is essential for IL-23 production in dendritic cells. These mechanisms would contribute to the development of strategies to control rheumatoid arthritis.
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[Journal Article] Pathogenesis of lupus -like nephritis through autoimmune antibody produced by CD180-negative B lymphocytes in NZBWF1 mouse.2012
Author(s)
Kazuko Fujita, Yoshikiyo Akasaka, Taku Kuwabara, Bing Wang, Kaoru Tanaka, Itaru Kamata, Tomoko Yokoo, Toshio Kinoshita, Ami Iuchi, Yuri Akishima-Fukasawa, Yukio Ishikawa, Motonari Kondo, and Toshiharu Ishii
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Journal Title
Immunology Letters
Volume: 144
Pages: 1-6
DOI
Peer Reviewed
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[Presentation] 妊娠マウスにおける子宮NK細胞の変化について2011
Author(s)
Akiko Takashima, Fumio Ishikawa, TakuKuwabara, Toshihiko Kinoshita, Terutaka Kakiuchi, and Motonari Kondo
Organizer
第40回日本免疫学会学術集会
Place of Presentation
幕張メッセ
Year and Date
2011-11-29
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