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. Author manuscript; available in PMC: 2009 Oct 21.
Published in final edited form as: Trends Immunol. 2009 Feb 13;30(3):131–141. doi: 10.1016/j.it.2008.12.003

Figure 4.

Figure 4

Model of the initiation and maintenance of autoimmune skin inflammation by LL37 in psoriasis. Skin injury and infections induce a rapid expression of the cathelicidin hCAPl8 in keratinocytes or infiltrated neutrophils. The mature peptide LL37 is cleaved from the precursor hCAP18 by Kalllikreins or proteinese 3. Subsequently LL37 combines with self-DNA released by damagad cells to form a complex. which triggers TLR9 in pDC to produce type 1 Interferons (IFNα and β). Type 1 IFNs trigger local maturation of myeloid dendritic cell to activate autoreactive Th1 or Th17 cells, resulting in the production of INF-γ,.IL-22 and IL-17. The sustained production of IL-22 and IL-17 leads to the expression of LL37 that forms a feedback loop to maintain inflammation in psoriasis.