The ectodomain of Toll-like receptor 9 is cleaved to generate a functional receptor

Sarah E. Ewald, Bettina L. Lee, Laura Lau, Katherine E. Wickliffe, Guo-Ping Shi, Harold A. Chapman and Gregory M. Barton ()
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Sarah E. Ewald: University of California, Berkeley, 405 Life Sciences Addition, Berkeley, California 94720-3200, USA
Bettina L. Lee: University of California, Berkeley, 405 Life Sciences Addition, Berkeley, California 94720-3200, USA
Laura Lau: University of California, Berkeley, 405 Life Sciences Addition, Berkeley, California 94720-3200, USA
Katherine E. Wickliffe: University of California, Berkeley, 405 Life Sciences Addition, Berkeley, California 94720-3200, USA
Guo-Ping Shi: Brigham and Women’s Hospital, Harvard Medical School, NRB-7, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA
Harold A. Chapman: and The Cardiovascular Research Institute, University of California, San Francisco, Box 0111, San Francisco, California 94143, USA
Gregory M. Barton: University of California, Berkeley, 405 Life Sciences Addition, Berkeley, California 94720-3200, USA

Nature, 2008, vol. 456, issue 7222, 658-662

Abstract: Autoimmunity: TLR9 activation The role of the Toll-like receptors TLR9 and TLR7 in mediating autoimmune disease to self nucleic acid is now well appreciated, yet the mechanisms preventing rampant autoimmunity remain largely unknown. Here Ewald et al. define the route by which TLR9 and TLR7 exit the endoplasmic reticulum and travel to endolysosomes in mouse macrophages and dendritic cells. TLR9 activation is shown to require proteolytic cleavage in the endolysosome. This may be a strategy to restrict receptor activation to endolysosomal compartments and prevent TLRs from responding to self nucleic acids.

Date: 2008
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DOI: 10.1038/nature07405

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