RGD Reference Report - Toll-like receptor 2 senses beta-cell death and contributes to the initiation of autoimmune diabetes. - Rat Genome Database

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Toll-like receptor 2 senses beta-cell death and contributes to the initiation of autoimmune diabetes.

Authors: Kim, HS  Han, MS  Chung, KW  Kim, S  Kim, E  Kim, MJ  Jang, E  Lee, HA  Youn, J  Akira, S  Lee, MS 
Citation: Kim HS, etal., Immunity. 2007 Aug;27(2):321-33. Epub 2007 Aug 16.
RGD ID: 2312684
Pubmed: PMID:17707128   (View Abstract at PubMed)
DOI: DOI:10.1016/j.immuni.2007.06.010   (Journal Full-text)

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 beta-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.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  

Objects Annotated

Genes (Rattus norvegicus)
Tlr2  (toll-like receptor 2)

Genes (Mus musculus)
Tlr2  (toll-like receptor 2)

Genes (Homo sapiens)
TLR2  (toll like receptor 2)


Additional Information