Toll-like receptor 2 senses beta-cell death and contributes to the initiation of autoimmune diabetesopen access
- Authors
- Kim, Hun Sik; Han, Myoung Sook; Chung, Kun Wook; Kim, Sunshin; Kim, Eunshil; Kim, Myoung Joo; Jang, Eunkyeong; Lee, Hyun Ah; Youn, Jeehee; Akira, Shizuo; Lee, Myung-Shik
- Issue Date
- Aug-2007
- Publisher
- CELL PRESS
- Keywords
- CELLIMMUNO; HIMDISEASE
- Citation
- IMMUNITY, v.27, no.2, pp.321 - 333
- Indexed
- SCIE
SCOPUS
- Journal Title
- IMMUNITY
- Volume
- 27
- Number
- 2
- Start Page
- 321
- End Page
- 333
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/179779
- DOI
- 10.1016/j.immuni.2007.06.010
- ISSN
- 1074-7613
- Abstract
- Although it is established that defective clearance and, hence, increased accumulation of apoptotic cells can lead to autoimmunity, the mechanism by which this occurs remains elusive. Here, we observed that apoptotic cells undergoing secondary necrosis but not intact apoptotic cells provoked substantial immune responses, which were mediated through the toll-like receptor 2 (TLR2) pathway. The development of autoimmune diabetes was markedly inhibited in Tlr2(-/-) mice but not in Tlr4(-/-) mice, showing that TLR2 plays an important role in the initiation of the disease. Apoptotic P-cell injury could stimulate the priming of diabetogenic T cells through a TLR2-dependent, but TLR4-independent, activation of antigen-presenting cells. These findings suggest that beta-cell death and its sensing via TLR2 may be an initial event for the stimulation of antigen-presenting cells and development of autoimmune diabetes.
- Files in This Item
-
Go to Link
- Appears in
Collections - 서울 의과대학 > 서울 해부·세포생물학교실 > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.