Nucleic Acid-sensing Tlrs As Modifiers of Autoimmunity.
From: Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA.
Journal of immunology (Baltimore, Md. : 1950)
- Publish Date: Nov 2006
- ISSN: 0022-1767
- Volume: 177
- Issue: 10
- Pages: 6573-8
- Medium: Print
- Language: English
- Citation (JAMA): Deane Jonathan A, Bolland Silvia, et al. Nucleic Acid-sensing Tlrs As Modifiers of Autoimmunity.. J. Immunol. Nov 2006;177:6573-8
Abstract
The immune system requires precise regulation of activating and inhibitory signals so that it can mount effective responses against pathogens while ensuring tolerance to self-components. Some of the most potent activation signals are triggered by innate immune molecules, particularly those in the TLR family. Recent studies have shown that engagement of TLRs plays a significant role in both innate and adaptive immunity. This review focuses on the ways that TLR function might contribute to the etiology of lupus-like syndromes in the context of an autoimmune-prone environment. By considering the sources, localization, and expression of both nucleic acids and the molecules that bind them, we discuss several ways that innate immunity can play a role in the development of systemic autoimmunity.
Mesh Headings (Keywords): Animals, Autoimmune Diseases, DNA, Humans, Immunity, Natural, RNA, Toll-Like Receptors
Check for Full Text / PubMed Unique Identifier (PMID): 17082566
This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.
Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.
The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.
