Pathogenesis of cutaneous lupus erythema associated with and without systemic lupus erythema

Abstract Cutaneous lupus erythematosus (CLE) can be an individual disease only involving skin, or presents as part of the manifestations of SLE. A small proportion of CLE may progress into SLE, however, the underlying pathogenic mediators remain elusive. By only including researches that clearly des...

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Bibliographic Details
Published in:Autoimmunity reviews 2017-07, Vol.16 (7), p.735-742
Main Authors: Zhang, Yu-ping, Wu, Jian, Han, Yan-fang, Shi, Zhen-rui, Wang, Liangchun
Format: Article
Language:English
Subjects:
Allergy and Immunology
Antibody
Cutaneous lupus erythematosus
Genetic and epigenetic susceptibility
Inflammatory cell
Inflammatory mediator
Skin inflammation
Systemic lupus erythematosus
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Summary:Abstract Cutaneous lupus erythematosus (CLE) can be an individual disease only involving skin, or presents as part of the manifestations of SLE. A small proportion of CLE may progress into SLE, however, the underlying pathogenic mediators remain elusive. By only including researches that clearly described if the subtypes of CLE presented by enrolled subjects was associated with or without SLE, we provided an overview of antibodies, inflammatory cells and inflammatory molecular mediators identified in blood and skin that were possibly involved in lupus skin damages. IgG autoantibodies are crucial for the development of CLE associated with SLE, but the circulating inflammatory cells and molecular mediators require further studies to provide definitive proof for their association with skin damages. Discoid lupus erythematosus (DLE) is the most common subtype of CLE. For DLE without associated with SLE (CDLE), it is lack of evidences if autoantibodies and circulating inflammatory cells are involved in the pathogenesis or not, but is clear that the cutaneous inflammatory infiltrates are dominated by Th1, but not Th17 cells in contrast to the various complex profile in SLE. As the major target cells in skin, keratinocytes may participate the pathophysiological process by increase cell apoptosis and the production of proinflammatory cytokines in SLE and CDLE. Insights into the similarities and differences of the pathogenesis of CLE and CLE associated with SLE will also improve our therapeutic strategies for CLE that is currently adopted from SLE, and prevent the progression of CLE to SLE by providing interventions within an appropriate window of disease development.
ISSN:1568-9972
1568-9972
DOI:10.1016/j.autrev.2017.05.009