OBJECTIVES: To investigate whether tumour necrosis factor alpha (TNFalpha) is expressed in subacute cutaneous lupus erythematosus (SCLE) skin lesions. METHODS: The in situ expression of TNFalpha in refractory lesional and non-lesional skin biopsy specimens from patients with SCLE was analysed using an immunohistochemical approach. At the time of biopsy these patients were receiving treatment with systemic medications such as antimalarial agents, immunosuppressive drugs, and thalidomide. Expression of TNFalpha was also evaluated in cutaneous lesions of patients with other inflammatory and neoplastic skin diseases as controls. RESULTS: The data showed that refractory lesional skin tissue from patients with SCLE displays a strongly positive distribution of TNFalpha, particularly within the epidermis. No prominent staining was seen in non-lesional skin from the same group of patients or in cutaneous lesions from the control group. CONCLUSIONS: These findings suggest that TNFalpha is localised and produced by epidermal cells within SCLE skin lesions and support its potential role in the pathogenesis of SCLE. The tissue localisation of TNFalpha may represent a potential therapeutic target providing a new perspective in the treatment of refractory skin lesions in patients with SCLE.
OBJECTIVES: To investigate whether tumour necrosis factor alpha (TNFalpha) is expressed in subacute cutaneous lupus erythematosus (SCLE) skin lesions. METHODS: The in situ expression of TNFalpha in refractory lesional and non-lesional skin biopsy specimens from patients with SCLE was analysed using an immunohistochemical approach. At the time of biopsy these patients were receiving treatment with systemic medications such as antimalarial agents, immunosuppressive drugs, and thalidomide. Expression of TNFalpha was also evaluated in cutaneous lesions of patients with other inflammatory and neoplastic skin diseases as controls. RESULTS: The data showed that refractory lesional skin tissue from patients with SCLE displays a strongly positive distribution of TNFalpha, particularly within the epidermis. No prominent staining was seen in non-lesional skin from the same group of patients or in cutaneous lesions from the control group. CONCLUSIONS: These findings suggest that TNFalpha is localised and produced by epidermal cells within SCLE skin lesions and support its potential role in the pathogenesis of SCLE. The tissue localisation of TNFalpha may represent a potential therapeutic target providing a new perspective in the treatment of refractory skin lesions in patients with SCLE.
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