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Editorial |

Type I Interferon in the Induction or Exacerbation of Dermatomyositis What This Observation Tells Us About the Naturally Occurring Disease

David F. Fiorentino, MD, PhD
Arch Dermatol. 2008;144(10):1379-1382. doi:10.1001/archderm.144.10.1379.
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Adverse events associated with medication use are a bane for physicians. However, when an adverse effect goes beyond an isolated clinical or laboratory finding and is instead a phenocopy of a naturally occurring disease state, we are presented with an opportunity to understand disease pathogenesis. The less common situation in which a disease state is reproduced with a naturally occurring biologic substance (ie, cytokine or hormone) makes even the most jaded of clinicians stand up and take note. The association of supraphysiologic amounts of an endogenous molecule with an induced disease state hardly provides physiologic proof of its connection in the spontaneously occurring disease, but it provides another level of evidence in a world in which the study of human disease rarely affords one with the opportunity to perform an in vivo experiment. It is with this level of interest and caution that we should approach the article in this issue of the Archives by Somani et al,1 in which the administration of interferon beta is associated with new-onset dermatomyositis.

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Figure 1.

Modes of interferon (IFN) induction and effects on leukocytes and parenchymal cells that promote systemic autoimmunity (reprinted with permission from Baccala et al30). Ag, indicates antigen; APRIL, a proliferation-inducing ligand; BLyS, B-lymphocyte stimulator; MHC, major histocompatibility complex; TH1, helper T cell type 1; and TLR, toll-like receptor.

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Figure 2.

Model for a 2-phase type I interferon (IFN) induction of autoimmunity. Various triggers for cellular death lead to debris uptake by immature dendritic cells (DC), which then produce small levels of type I IFN sufficient to activate myeloid DCs (mDC). The mDCs then activate autoreactive B cells (B) and T cells (T), resulting in immune complexes. These nucleic acid–containing immune complexes activate plasmacytoid DCs (pDC), which produce high levels of type I IFN to amplify the cycle (reprinted with permission from Baccala et al30). APRIL indicates a proliferation-inducing ligand; BLyS, B lymphocyte stimulator; MHC, major histocompatibility complex; and TLR, toll-like receptor.

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