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Curr Opin Immunol. 2011 Feb;23(1):3-9. doi: 10.1016/j.coi.2010.11.006. Epub 2010 Dec 14.

Nucleic acid sensing Toll-like receptors in autoimmunity.

Author information

1
Division of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, 405 Life Sciences Addition, Berkeley, CA 94720-3200, USA. see@stanford.edu

Abstract

Trafficking and activation of the nucleic acid sensing TLRs is subject to unique regulatory requirements imposed by the risk of self-recognition. Like all TLRs these receptors traffick through the Golgi, however, access to the secretory pathway is controlled by a binding partner present in the ER. Receptor activation in the endolysosome is regulated through a proteolytic mechanism that requires activity of compartment-resident proteases, thereby preventing activation in other regions of the cell. Advances in our understanding of the cell biology of these receptors have been paralleled by efforts to understand their precise roles in autoimmunity. Mouse models have revealed that TLR7 and TLR9 make unique contributions to the types of self-molecules recognized in disease and possibly disease severity. Currently, methods of inhibiting TLR7 and TLR9 are being tested in clinical trials for systemic lupus erythamatosus.

PMID:
21146971
PMCID:
PMC3057394
DOI:
10.1016/j.coi.2010.11.006
[Indexed for MEDLINE]
Free PMC Article

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