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R Treudler

Publications and source records attributed to R Treudler.

22 records · Page 2Linked to original sources

Enhanced interaction of patients' lymphocytes with human dermal microvascular endothelial cell cultures in active Adamantiades-Behçet disease.

BACKGROUND AND DESIGN: To elucidate the role of lymphocyte/endothelial cell interactions in patients with Adamantiades-Behçet disease (ABD), we studied 16 patients of German and Turkish nationality (aged 18-57 years), all with active ABD, and 12 healthy volunteers (controls) of similar age and nationality. Peripheral blood lymphocytes (PBL) of patients were coincubated with human dermal microvascular endothelial cells (HDMEC) and human keratinocytes (HK) in vitro; interactions of PBL with HDMEC and HK were investigated using an established fluorometric assay. Interactions of patients' PBL with HDMEC, HK, or both were the main outcome measures. RESULTS: A significant increase of fluorescence with increasing PBL/HDMEC ratios was seen in patients and controls (P < .001); patients showed a significantly higher increase of fluorescence at higher PBL/HDMEC ratios (P < .05). The PBL/HK coincubation did not show significant alterations compared with the basal fluorescence signals of HK monolayers alone. Peripheral blood lymphocyte and HDMEC fluorescence values that were more than 2 SDs of controls (defined as positive result of assay) were found in a significantly higher number of patients with 2 or more active symptoms at the time of investigation (83%) compared with patients with only 1 active symptom (10%) (P = .008). Other clinical data did not correlate with the results of the PBL/HDMEC coincubation assay. CONCLUSIONS: Our results indicate enhanced in vitro interaction of PBL from patients with ABD with HDMEC, which was additionally shown to be a marker of the activity of the disease.

Adolescent↗

[Adamantiades-Behçet disease. Therapeutic administration of systemic recombinant interferon-alpha-2a].

The effect of systemic recombinant interferon alpha-2a (rIFN-alpha-2a) on the mucocutaneous lesions in Adamantiades-Behçet's disease was assessed in ten patients with the mucocutaneous type of the disease. rIFN-alpha-2a was applied subcutaneously at a dose of 9 x 10(6) IU three times a week for 6 months. Five patients showed a significant reduction in the number, severity, duration and frequency of their mucocutaneous lesions during the treatment compared with the pretreatment phase, whereas in two patients a complete remission and in three patients a partial remission was achieved. In two patients, one with complete and one with partial remission, recurrence of the cutaneous symptoms occurred shortly after discontinuation of the treatment. Renewed administration of rIFN-alpha-2a again led to remission of the symptoms. In another patient with initial partial remission followed by exacerbation, interferon alpha antibodies were detected and the patient responded again when 15 x 10(6) IU rIFN-alpha-2a was administered three times a week. Three patients did not show any change in the characteristics of their lesions, while two patients experienced progression of their disease during treatment. Side-effects were generally mild and well tolerated, but the treatment was discontinued earlier than planned in one patient because of fatigue, myalgia, hypotonus and diarrhoea. Since the classical treatments are generally unsatisfactory, the results of the present study justify the administration of systemic rIFN-alpha-2a in the treatment of the mucocutaneous type of Adamantiades-Behçet's disease.

Adult↗

Langerhans cells do not express alternative macrophage activation-associated CC chemokine (AMAC)-1.

We have cloned a novel human CC chemokine, alternative macrophage activation-associated CC chemokine (AMAC)-1 that is highly homologous to macrophage inflammatory protein (MIP)-1alpha. In contrast to MIP-1alpha, AMAC-1 is induced in macrophages by Th2-associated cytokines IL4, IL13, and IL10 in vitro; in addition, AMAC-1 is expressed by Th1-suppressive alveolar macrophages in vivo. Surprisingly, however, AMAC-1 is also expressed by GM-CSF-induced, in vitro monocyte-derived dendritic cells when treated by IL4. Here, we present a detailed analysis of AMAC-1 expression in monocyte-derived dendritic cells in vitro and show that the prime dendritic cells in vivo, i.e. epidermal Langerhans cells, do not express AMAC-1 mRNA. In conclusion, AMAC-1 is a novel CC chemokine whose Th2-associated expression pattern in alternatively activated suppressor macrophages in vivo and in vitro and its absence from epidermal Langerhans cells in vivo suggest that it may be involved in inhibition of Th1 reactions and in tolerance induction.

Chemokines, CC↗