Nicole Baumgarth1 & Charles L. Bevins2
The antimicrobial peptide LL37 is essential for normal immune responses to infection or tissue injury. But in the autoimmune skin disorder psoriasis, LL37 propagates disease by forming complexes with host DNA.
The innate (nonspecific) immune system is responsible for detecting pathogens and inducing effector molecules to coordinate subsequent immune responses and combat infection. Genes encoding the receptors of innate immunity are hard-wired in the host genome, and honed to near perfection by the selective pressures of evolution to respond only to non-self targets. When tolerance (non-responsiveness to self) is broken, this can result in autoimmune disease. On page 564 of this issue, Lande et al.1 report a costly glitch in the innate immune response that seems to underlie the development of the common autoimmune skin disease psoriasis∗.
Psoriasis is marked by chronic inflammation and excessive proliferation and turnover of the keratinocyte skin cells, which result in characteristic silvery white scaly patches overlying the inflamed skin2. The specific causes of psoriasis are unknown, but environmental triggers — including bacterial skin infections, mild trauma and stress — and strong genetic factors underlie the development of the disease. At a cellular level, an accumulation of inflammatory cells largely consisting of activated T cells and antigen-presenting cells, particularly plasmacytoid dendritic cells (pDCs), precedes other aspects of the disease's pathology. Therefore, psoriasis is currently thought of as an autoimmune inflammatory disorder, but what initiates and perpetuates it has remained enigmatic.
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