Lupus erythematosus panniculitis is a rare disease characterized by deep subcutaneous nodules, most commonly localized on the upper limbs and face. Unique clinical presentations, such as linear configuration or ‘overlap’ forms between lupus erythematosus panniculitis and localized scleroderma have been reported. We present here the clinical characteristics, course and laboratory findings of 2 patients having linear lupus erythematosus panniculitis with localized scleroderma-like changes. The 2 patients (of the 14 patients with lupus erythematosus panniculitis seen by us since 1990) were females with a young age at the onset of disease (median, 25 years). In 1 case, evolution into systemic lupus erythematosus with severe renal involvement occurred whereas the other patient, who had a spontaneous abortion and exhibited anticardiolipin antibodies, should be followed and screened for the emergence of antiphospholipid syndrome. Thus, the clinical behavior of this variant seems to be more aggressive, as compared with the usual course of lupus erythematosus panniculitis, which is considered to be a benign disease, although some reports have suggested that its prognosis is not always favorable. The linear distribution could be the clinical hallmark of such a unique, ‘sclerodermic’ subset of lupus erythematosus panniculitis.
To understand the mechanisms involved in immunological tolerance to skin-associated proteins, we have developed trangenic (Tg) mice that express a model self antigen, membrane-bound ABSTRACTS 125 FS01.3 Disperse (yes), orange (yes), 3 (no): what do we test in textile dye dermatitis?Para-phenylenediamine (PPD), an arylamine dye, is a strong allergen causing allergic contact dermatitis. Cytokines such as TNF-a and IL-1beta are key mediators in the initiation of this reaction. Both cytokines are predominantly produced by stimulated monocytes and macroghages. We investigated the responses of PPD and Bandrowski's base (BB), an autoxidation product of PPD in human monocytes. We isolated monocytes from healthy volunteers and incubated them with the allergens. TNF-a and IL-1beta mRNA expression and protein levels were estimated after 45 min, 2 h, 4 h and 24 h after allergen contact. IL-1beta and TNF-alpha were measured in cell culture supernatants by ELISA (n ¼ 7) and mRNA expression was determined by real-time RT-PCR. We found that PPD reduced TNF-a protein secretion by 20-69.9% (n ¼ 6). Further, IL-1beta levels were decreased by 44-98%. The same tendency was found studying IL-1beta and TNF-a mRNA steady state levels (n ¼ 3; 1 h incubation). These effects were substance-specific and not found for PPD derivatives nor for the autoxidation product BB. These findings suggest that PPD may specifically modify immune responses by directly infering with the cellular proinflammatory cytokine network.
To understand the mechanisms involved in immunological tolerance to skin-associated proteins, we have developed trangenic (Tg) mice that express a model self antigen, membrane-bound ABSTRACTS 125 FS01.3 Disperse (yes), orange (yes), 3 (no): what do we test in textile dye dermatitis?Para-phenylenediamine (PPD), an arylamine dye, is a strong allergen causing allergic contact dermatitis. Cytokines such as TNF-a and IL-1beta are key mediators in the initiation of this reaction. Both cytokines are predominantly produced by stimulated monocytes and macroghages. We investigated the responses of PPD and Bandrowski's base (BB), an autoxidation product of PPD in human monocytes. We isolated monocytes from healthy volunteers and incubated them with the allergens. TNF-a and IL-1beta mRNA expression and protein levels were estimated after 45 min, 2 h, 4 h and 24 h after allergen contact. IL-1beta and TNF-alpha were measured in cell culture supernatants by ELISA (n ¼ 7) and mRNA expression was determined by real-time RT-PCR. We found that PPD reduced TNF-a protein secretion by 20-69.9% (n ¼ 6). Further, IL-1beta levels were decreased by 44-98%. The same tendency was found studying IL-1beta and TNF-a mRNA steady state levels (n ¼ 3; 1 h incubation). These effects were substance-specific and not found for PPD derivatives nor for the autoxidation product BB. These findings suggest that PPD may specifically modify immune responses by directly infering with the cellular proinflammatory cytokine network.
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