Circulating skin-homing T cells in atopic dermatitis. Selective up-regulation of HLA-DR, interleukin-2R, and CD30 and decrease after combined UV-A and UV-B phototherapy.
BACKGROUND
As the cutaneous lymphocyte-associated antigen appears to detect circulating T cells that migrate to the skin in atopic dermatitis but not T cells that migrate to mucosal sites in allergic asthma and rhinitis, we investigated T-cell activation markers and CD30 on the cutaneous lymphocyte-associated antigen-positive circulating T-cell subset in atopic dermatitis to see whether these markers are different from those in normal controls and related to disease activity.


METHODS
Open study.


METHODS
University referral center.


METHODS
Twelve patients with atopic dermatitis and 12 healthy controls.


METHODS
Combined UV-A and UV-B treatment for 2 months.


METHODS
Percentage of circulating cutaneous lymphocyte-associated antigen-positive T cells that express HLA-DR, interleukin-2 receptor, CD69, CD71, and CD30 (triple-color flow cytometric analysis). Clinical score, Dermatology Life Quality Index, pruritus score, and consumption of topical corticosteroids were determined.


RESULTS
Increased relative numbers of cutaneous lymphocyte-associated antigen-positive T cells expressing HLA-DR, interleukin-2 receptor, and CD30 were found in patients with atopic dermatitis before treatment. Treatment with UV-A and UV-B was associated with clinical improvement and a decrease of levels of HLA-DR, interleukin-2 receptor, and CD30 in cutaneous lymphocyte-associated antigen-positive T cells. HLA-DR on cutaneous lymphocyte-associated antigen-positive T cells correlated significantly with the clinical score.


CONCLUSIONS
Expression of HLA-DR and interleukin-2 receptor is a sensitive marker of disease activity in atopic dermatitis. Apart from giving information on disease activity in atopic dermatitis, the availability of skin-seeking T cells in the blood offers the opportunity to obtain further information on T cells that may have effector function in the skin.
Piletta
P A
PA
Department of Dermatology, Hôpital Cantonal, University of Geneva, Switzerland.
Wirth
S
S
Hommel
L
L
Saurat
J H
JH
Hauser
C
C
D000293:Adolescent; D000328:Adult; D000945:Antigens, Differentiation, T-Lymphocyte; D000951:Antigens, Neoplasm; D003876:Dermatitis, Atopic / Q000276:immunology* / Q000532:radiotherapy; D005260:Female; D006684:HLA-DR Antigens / Q000378:metabolism*; D006801:Humans; D017730:Ki-1 Antigen / Q000378:metabolism*; D008297:Male; D008562:Membrane Glycoproteins / Q000378:metabolism*; D008875:Middle Aged; D015375:Receptors, Interleukin-2 / Q000378:metabolism*; D016201:Receptors, Lymphocyte Homing / Q000378:metabolism*; D012867:Skin / Q000276:immunology*; D016176:T-Lymphocyte Subsets; D014467:Ultraviolet Therapy; D015854:Up-Regulation / Q000528:radiation effects
D000945:Antigens, Differentiation, T-Lymphocyte; D000951:Antigens, Neoplasm; C063419:CTAGE1 protein, human; D006684:HLA-DR Antigens; D017730:Ki-1 Antigen; D008562:Membrane Glycoproteins; D015375:Receptors, Interleukin-2; D016201:Receptors, Lymphocyte Homing