Efficacy of ultraviolet A1 phototherapy on the expression of bcl-2 in atopic dermatitis and cutaneous T-cell lymphoma in vivo:: a comparison study

被引:22
作者
Breuckmann, F [1 ]
von Kobyletzki, G [1 ]
Avermaete, A [1 ]
Kreuter, A [1 ]
Altmeyer, P [1 ]
机构
[1] Ruhr Univ Bochum, Dept Dermatol Clin & Expt Photodermatol, D-44791 Bochum, Germany
关键词
apoptosis; atopic dermatitis (AD); bcl-2; cutaneous T-cell lymphoma (CTCL); UVA1; phototherapy;
D O I
10.1034/j.1600-0781.2002.02740.x
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Background/Purpose: Atopic dermatitis (AD) is characterized immunohistochemically by a high number of skin infiltrating T-helper cells (CD4 (+) ). In most cases cutaneous T-cell lymphoma (CTCL) is characterized by a malignant proliferation of CD4 (+) T-helper lymphocytes. The purpose of our study was to evaluate the extent of anti-apoptotic effects in patients suffering from AD or CTCL, respectively, which may contribute to the prolonged inflammation. Furthermore, we investigated whether medium-dose ultraviolet A1 (UVA1) phototherapy is able to modulate the expression of bcl-2 within the dermal inflammatory infiltrate. Methods: In order to enumerate bcl-2 (+) cells pre- and post-therapeutic punch skin biopsies of ten patients with AD and five patients with CTCL were stained immunohistochemically for features of apoptosis using a monoclonal antibody detecting bcl-2. Results: Both AD and CTCL sections revealed a high percentage of bcl-2 (+) cells within the dermal perivascular infiltrate before therapy. After the successful treatment using medium-dose UVA1 phototherapy this percentage could be decreased significantly. Conclusion: Both T-cell-derived skin diseases exhibit an increased pre-therapeutic number of bcl-2 (+) cells. After medium-dose UVA1 phototherapy the substantial improvement of the skin condition was linked to a significant decrease of the dermal bcl-2 (+) cell count. Moreover, we could demonstrate a remarkable correlation referring to the decrease and staining pattern of bcl-2 between these two groups as well as within each group. Because the bcl-2 protein is known to act as an apoptosis inhibitor, its pre-therapeutic increase may provide the persistent cutaneous inflammatory reaction in T-cell-derived skin diseases. Additionally, the post-therapeutic reduction of bcl-2 (+) cells might represent a key mechanism of medium-dose UVA1 phototherapy.
引用
收藏
页码:217 / 222
页数:6
相关论文
共 25 条
[1]  
[Anonymous], ACTA DERM VENERE S92, DOI [10.2340/00015555924447, DOI 10.2340/00015555924447]
[2]  
BREUCKMANN F, 2000, J EUR ACAD DERMAT S1, V14, P122
[3]   Modulation of UVA-induced lipid peroxidation and suppression of UVB-induced ornithine decarboxylase response by all-trans-retinoic acid in human skin fibroblasts in vitro [J].
Francz, PI ;
Conrad, J ;
Biesalski, HK .
BIOLOGICAL CHEMISTRY, 1998, 379 (10) :1263-1269
[4]  
GILCHREST BA, 1976, CANCER, V38, P683, DOI 10.1002/1097-0142(197608)38:2<683::AID-CNCR2820380210>3.0.CO
[5]  
2-V
[6]  
Godar D E, 1994, Cell Death Differ, V1, P59
[7]   Activation of transcription factor AP-2 mediates UVA radiation- and singlet oxygen-induced expression of the human intercellular adhesion molecule 1 gene [J].
GretherBeck, S ;
OlaizolaHorn, S ;
Schmitt, H ;
Grewe, M ;
Jahnke, A ;
Johnson, JP ;
Briviba, K ;
Sies, H ;
Krutmann, J .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (25) :14586-14591
[8]   PHENOTYPIC CHARACTERIZATION OF CUTANEOUS T-CELL LYMPHOMA - USE OF MONOCLONAL-ANTIBODIES TO COMPARE WITH OTHER MALIGNANT T-CELLS [J].
HAYNES, BF ;
METZGAR, RS ;
MINNA, JD ;
BUNN, PA .
NEW ENGLAND JOURNAL OF MEDICINE, 1981, 304 (22) :1319-1323
[9]  
HEIJDEN FL, 1991, J INVEST DERMATOL, V97, P389
[10]   A RANDOMIZED TRIAL COMPARING COMBINATION ELECTRON-BEAM RADIATION AND CHEMOTHERAPY WITH TOPICAL THERAPY IN THE INITIAL TREATMENT OF MYCOSIS-FUNGOIDES [J].
KAYE, FJ ;
BUNN, PA ;
STEINBERG, SM ;
STOCKER, JL ;
IHDE, DC ;
FISCHMANN, AB ;
GLATSTEIN, EJ ;
SCHECHTER, GP ;
PHELPS, RM ;
FOSS, FM ;
PARLETTE, HL ;
ANDERSON, MJ ;
SAUSVILLE, EA .
NEW ENGLAND JOURNAL OF MEDICINE, 1989, 321 (26) :1784-1790