Detection of type 1 cytokines in discoid lupus erythematosus

Backgrounds: Although multiple studies suggest a dysregulated T-cell cytoki ne production in systemic lupus erythematosus, the cytokine profile in disc oid lupus erythematosus (DLE) lesions is unknown. Objectives: To characterize the cytokine profile in DLE by immunohistochemi cal and molecular methods, and to investigate the role of cytokines in the pathogenesis of DLE. Design: Patients were evaluated clinically, and biopsy specimens of lesiona l skin were examined by light microscopy. Reverse transcriptase-polymerase chain reaction and immunohistochemical analysis were performed on 11 biopsy specimens. We investigated the presence of interleukin (IL) 2, interferon gamma (IFN-gamma), IL-4, tumor necrosis factor alpha, (TNF-alpha) and IL-1 beta messenger RNA (mRNA) in 8 biopsy specimens of DLE and compared it with 3 biopsy specimens of normal skin. Setting: Academic referral research hospital. Patients: Eight consecutive patients with a clinical and histologic diagnos is of DLE. Results: Localized DLE was found in 7 patients and widespread in 1. During the 4 years of the investigation, none of the patients developed systemic l upus erythematosus. We found significantly elevated levels of IL-2 and IFN- gamma mRNA in all 8 biopsy specimens of DLE; in contrast, no transcripts of IL-2 or IFN-gamma were detected in 3 biopsy specimens of normal skin (P<.0 1). Similarly, elevated levels of TNF-<alpha> mRNA were detected in 8 DLE b iopsy specimens of normal skin (P<.01). No IL-5 or IL-1<beta> mRNA was dete cted in 8 biopsy specimens of DLE lesional skin and 3 biopsy specimens of n ormal patient skin. Immunohistochemical analysis showed increased staining for IL-2 and IFN-gamma receptors, while no detectable IL-4 receptor was fou nd. No cytokine mRNA or cytokine receptor protein was detected in biopsy sp ecimens of normal skin. Conclusions: These findings suggest that DLE is associated with type 1 cyto kines characterized by the expression of IL-2 and IFN-gamma. Type 1 cytokin es may be critical for induction, development, and maintenance of DLE.