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217 Prior sun exposure and skin-specific auto-antibodies are associated with skin disease in systemic lupus erythematosus
  1. T Khosravi-Hafshejani1,
  2. M Ghoreishi2,
  3. A Kariminia3,
  4. S Kalia2,
  5. A Avina-Zubieta4,
  6. J Reynolds4 and
  7. JP Dutz2
  1. 1University of British Columbia, Undergraduate Medical Program- Faculty of Medicine, Vancouver, Canada
  2. 2University of British Columbia, Dermatology and Skin Science, Vancouver, Canada
  3. 3University of British Columbia, Pediatrics- Division of Haematology and Oncology, Vancouver, Canada
  4. 4University of British Columbia, Medicine- Division of Rheumatology, Vancouver, Canada

Abstract

Background and aims Almost 80% of systemic lupus erythematosus (SLE) patients manifest lupus-specific skin lesions. A pathogenic link between skin inflammation and SLE has been proposed. We hypothesised that skin-directed antibodies are present in SLE and are associated with a history of significant sun-exposure.

Methods Blood was collected from three patient populations; SLE with a history of lupus-specific skin lesions as cases (n=15), SLE without a history of skin lesions (n=7) and atopic dermatitis (n=6) as controls. Serum antid-esmoglein-3 antibodies were measured by ELISA. Peripheral blood mononuclear cells were analysed by flow cytometry. Patients completed a scored questionnaire addressing sun exposure history prior to disease onset. The questionnaire, flow cytometry and ELISA results were analysed using Mann-Whitney test.

Results Questionnaire responses indicate increased sun exposure prior to disease onset in SLE patients with skin disease when compared to SLE patients without skin disease (median score=60 versus 32, respectively; p<0.05). Anti-desmoglein-3 auto-antibody levels were higher in the serum of SLE patients with skin disease than in patients without skin disease (median=0.571 versus 0.123 IU, respectively; p<0.05). T-follicular helper (TFH) cells stimulate B-cells to produce auto-antibodies via IL-21. There was a trend to enhanced IL-21 production in SLE with skin lesions compared to SLE without skin (median=34 versus 19%, respectively).

Conclusions SLE patients with skin disease have a history of higher antecedent sun exposure consistent with the hypothesis that sun exposure is an environmental trigger. The resulting immune activation of the skin may be reflected in aberrant skin-specific antibody production and heightened IL-21 secretion by TFH cells.

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