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Nucleic Acid-Sensing TLRs as Modifiers of Autoimmunity¹

Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852

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.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was funded by the Intramural Research Program of the National Institute of Allergy and Infectious Diseases.

² Address correspondence and reprint requests to Dr. Silvia Bolland, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, 12441 Parklawn Drive, Room 217, Rockville, MD 20852. E-mail address: sbolland{at}nih.gov

³ Abbreviations used in this paper: ko, knockout; RNP, ribonucleoprotein.

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