Increased Cutaneous Lymphocyte Antigen (CLA) +T Cells in the Peripheral Blood of Children with Severe Atopic Dermatitis / 소아알레르기및호흡기학회지

PURPOSE: Skin-homing T cells expressing cutaneous lymphocyte antigen (CLA) are known to be important in the pathogenesis of atopic dermatitis (AD). So far, there have been few reports on the peripheral lymphocyte subpopulations expressing CLA, especially in children with AD. METHODS: We investigated the peripheral blood lymphocyte subpopulations expressing CLA in children with severe AD andcontrol subjects to identify which proportions of circulating CLA+ T cells were expanded in atopic dermatitis. We assayed the peripheral blood lymphocyte subpopulation with flow cytometry in 15 children with severe chronic lichenified skin lesions and 12 control subjects who had no symptoms of atopic dermatitis. The expressions of peripheral blood CD4+CLA+ T cells and CD3+CLA+ T cells were significantly increased in children with AD compared with those in control subjects, whereas there was no significant difference of CD8+CLA+ T cells between the two groups. RESULTS: The expressions of CD3+ T cells, CD4+ T cells, and CD8+ T cells showed no significant differences between children with AD and control subjects. CONCLUSION: These findings suggest that circulating CD4+CLA+ T cells play an important role in the pathogenesis of chronic severe AD in children.

Changes in Peripheral Blood T Cells after Treatment of Cyclosporine in Children with Severe Atopic Dermatitis / 소아알레르기및호흡기학회지

BACKGROUND: Skin-homing T cells expressing cutaneous lymphocyte antigen (CLA) are known to be important in the pathogenesis of atopic dermatitis (AD). Cyclosporine is known as an effective treatment for severe atopic dermatitis, which controls the cytokine production from T cells and regulates the activation of T cells. There have been no reports about the changes of circulating CLA+ T cells after the treatment of cyclosporine in AD. The aim of this study was to evaluate the clinical outcome and the changes of CLA+ T cells after treatment of cyclosporine in childhood AD. METHODS: Ten children with severe AD were treated with cyclosporine (5 mg/kg/day) for six weeks. Clinical outcome was monitored by the SCORAD index. We assayed the peripheral blood T lymphocyte subpopulation including CLA+ T cells with flow cytometry. RESULTS: The SCORAD index decreased significantly after treatment (P< 0.05). CD4+CLA+ T cells and CD3+CLA+ T cells were significantly decreased after the treatment of cyclosporine. (P< 0.05) But CD3+ T cells, CD4+ T cells and CD8+ T cells were not changed. CONCLUSION: Cyclosporine is effective to control severe AD in children and decreases CD4+CLA+ T cells, which may be important in the pathogenesis of AD.

Pseudo-Kaposi Sarcoma:Differential Diagnosis from Kaposi Sarcoma

BACKGROUND: Pseudo-Kaposi sarcoma mimicks Kaposi sarcoma, both clinically and histopathologically. These conditions are due to congenital (Stewart-Bluefarb syndrome) or acquired (Mali) vascular malformations. OBJECTIVES: The purposes of this study were aimed at evaluating the clinical and histopathological characteristics of pseudo-Kaposi sarcoma and finding differential diagnostic tools from Kaposi sarcoma. METHODS: Clinical information of 7 patients with pseudo-Kaposi sarcoma diagnosed in Asan Medical Center from 1989 to 1999 was obtained from the medical records and clinical follow-ups. We re-evaluated 10 biopsy specimens obtained from them and immunohistochemical studies for cutaneous lymphocyte antigen (CLA), CD34, vimentin, and factor VIII were performed with the standard streptavidin-biotin method using paraffin-embedded tissue specimens of 7 pseudo-Kaposi sarcomas and 3 Kaposi sarcomas. In addition, we examined whether human herpesvirus 8 (HHV8) was detected in 3 patients by polymerase chain reaction (PCR). RESULTS: Six male and one female patients were included. Mean age was 36.3 years. Three patients were classified into Mali type and the other four patients were into Stewart-Bludfarb type. Histopathological examinations revealed capillary proliferation in the upper dermis, perivascular infiltrate of inflammatory cells, extravasated red blood cells, and fibrosis of dermis. Anti-factor VIII and CD34 stained endothelial cells only. CLA was expressed in lymphocytic infiltrate in the epidermis and dermis of pseudo-Kaposi sarcoma, whereas it was negative in Kaposi sarcoma. PCR for HHV 8 showed negative results. CONCLUSIONS: Pseudo-Kaposi sarcoma is an uncommon entity with characteristic clinical and histopathological features. Differential diagnosis between Pseudo-Kaopsi sarcoma and Kaposi sarcoma is important. We suggest that detection of HHV 8 by PCR and imunohistochemical study for CLA may be effective tools in the differential diagnosis between them.