Clinical manifestations of cutaneous lupus erythematosus are diverse and different subtypes of the disease have been defined. It is characteristic for lupus skin inflammation that a significant activation of innate interferon pathways is observable. Endogenous molecules indicative for tissue damage (damage-associated molecular patterns [DAMPs]) show cytokine-like properties once released from intracellular compartments and these DAMPs have been shown to influence the course of inflammatory responses. Cytokines including TNF-α and IL-1 family members significantly contribute to the chronic inflammatory phenotype and, in combination with DAMPs, impact on the activation of innate interferons. A better understanding of the deregulated cytokine network in cutaneous lupus erythematosus patients with distinct disease phenotypes and genetic backgrounds is of high importance and a prerequisite for recommending and developing more individualized therapeutic strategies.
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Wittmann et al. (2011) studied this question.
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