Abstract:
:Plasmacytoid dendritic cells (pDCs) sense viral and microbial DNA through endosomal Toll-like receptors to produce type 1 interferons. pDCs do not normally respond to self-DNA, but this restriction seems to break down in human autoimmune disease by an as yet poorly understood mechanism. Here we identify the antimicrobial peptide LL37 (also known as CAMP) as the key factor that mediates pDC activation in psoriasis, a common autoimmune disease of the skin. LL37 converts inert self-DNA into a potent trigger of interferon production by binding the DNA to form aggregated and condensed structures that are delivered to and retained within early endocytic compartments in pDCs to trigger Toll-like receptor 9. Thus, our data uncover a fundamental role of an endogenous antimicrobial peptide in breaking innate tolerance to self-DNA and suggest that this pathway may drive autoimmunity in psoriasis.
journal_name
Naturejournal_title
Natureauthors
Lande R,Gregorio J,Facchinetti V,Chatterjee B,Wang YH,Homey B,Cao W,Wang YH,Su B,Nestle FO,Zal T,Mellman I,Schröder JM,Liu YJ,Gilliet Mdoi
10.1038/nature06116subject
Has Abstractpub_date
2007-10-04 00:00:00pages
564-9issue
7162eissn
0028-0836issn
1476-4687pii
nature06116journal_volume
449pub_type
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