T lymphocytes and dendritic cells are activated by the deletion of peroxiredoxin II (Prx II) gene
- Authors
- Moon, EY; Noh, YW; Han, YH; Kim, SU; Kim, JM; Yu, DY; Lim, JS
- Issue Date
- Feb-2006
- Publisher
- ELSEVIER SCIENCE BV
- Keywords
- peroxiredoxin II (Prx II); reactive oxygen species (ROS); dendritic cell; T lymphocyte
- Citation
- IMMUNOLOGY LETTERS, v.102, no.2, pp 184 - 190
- Pages
- 7
- Journal Title
- IMMUNOLOGY LETTERS
- Volume
- 102
- Number
- 2
- Start Page
- 184
- End Page
- 190
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/15179
- DOI
- 10.1016/j.imlet.2005.09.003
- ISSN
- 0165-2478
1879-0542
- Abstract
- Peroxiredoxin II (Prx II) is a member of antioxidant enzyme family and it plays a protective role against oxidative damage. Constitutive production of endogenous reactive oxygen species was detected in spleen and bone marrow cells lacking Prx II. Here, we investigated the role of Prx II in immune responses. The total number of splenocytes (especially, the population of S-phase cells and CD3(+) T cells) was significantly higher in Prx II-/- mice than in wild type. Number of peripheral blood mononuclear cells (PBMCs) in Prx II-/- mice was also higher than wild type. Differentiation of Prx II-/- mouse bone marrow cells into CDIIc-positive dendritic cells was greater than that of wild type. Transplantation of Prx II-/- bone marrow cells into wild type mice increased PBMCs in blood and bone marrow-derived dendritic cells. Prx II deletion enhances concanavalin A (ConA)-induced splenocyte proliferation and mixed lymphocyte reaction (MLR) activity of bone marrow-derived CDIIc-positive dendritic cells to stimulate recipient splenocytes. Collectively, these data suggest that Prx II inhibits the immune cell responsiveness, which may be regulated by scavenging the low amount of reactive oxygen species (ROS). (c) 2005 Elsevier B.V. All rights reserved.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - 이과대학 > 생명시스템학부 > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.