Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2009 Mar;67(3):487-93.

[Role of TLR-dependent and independent pathways in autoimmunity]

[Article in Japanese]
Affiliations
  • PMID: 19280921
Review

[Role of TLR-dependent and independent pathways in autoimmunity]

[Article in Japanese]
Yutaro Kumagai et al. Nihon Rinsho. 2009 Mar.

Abstract

Innate immune system senses invading pathogens through their molecular patterns and elicits pleiotropic immune responses including production of proinflammatory cytokines and antigen presentation. However, the system could sense host endogenous molecules and elicits immune response against self resulting into autoimmunity. In this regard, Toll-like receptor (TLR) is involved in several autoimmune diseases such as systemic lupus erythematosus. Recently identified TLR-independent pathways are revealed also to have roles in autoimmunity as well as TLR. Innate recognition of intracellular DNA, of which receptor is still unknown, is involved in several autoimmune diseases through its endogenous ligand. Moreover, Nod-like receptors play important role in chronic inflammatory diseases like gout and Crohn's disease. In this review, the authors described the role of innate recognition system in autoimmunity, emphasizing on their molecular mechanism.

PubMed Disclaimer

LinkOut - more resources