Fc epsilon receptor II/CD23+ lymphocytes in atopic dermatitis. III. Aberrant control in the in vitro expression of Fc epsilon RII/CD23 on peripheral blood T cells in atopic dermatitis.
In vitro Fc epsilon RII expression was examined in patients with atopic dermatitis, those with non-atopic eczematous dermatitis and normal individuals following stimulation of peripheral blood cells with recombinant IL-4 (rIL-4), phytohaemagglutinin (PHA), or PHA plus rIL-2. At various days cells were stained with MoAbs to human lymphocyte Fc epsilon RII and to lymphoid cell-surface antigens and analysed by flow cytometry. rIL-4, but not rIL-2, specifically induced Fc epsilon RII on T cells as well as B cells in atopic dermatitis, eczematous dermatitis and normal individual groups. Both atopics and non-atopics generated comparable proportions of Fc epsilon RII+ T cells (T epsilon cells), whereas the frequency of B cells bearing Fc epsilon RII(B epsilon cells) was significantly higher in patients with extensive atopic dermatitis than in those with mild atopic dermatitis and other subjects. Comparable levels of T epsilon cells were detected in both atopic and non-atopic donors following stimulation of peripheral blood cells with PHA or pre-activation of the cells with PHA plus subsequent incubation with rIL-2. Whereas both CD8+ and CD4+ subsets were present in T epsilon cell populations induced specifically by rIL-4, PHA and PHA plus rIL-2, patients with atopic dermatitis had a greater tendency for Fc epsilon RII expression on CD8+ T cells compared with patients with eczematous dermatitis and normal individuals. Recombinant interferon-gamma (rIFN-gamma), but not rIFN-alpha or prostaglandin E2 (PGE2), suppressed the generation of T epsilon cells by rIL-4 in atopics and non-atopics to the same degree. These results suggest the aberrant control of Fc epsilon RII expression on T cells, especially those bearing CD8, in atopic dermatitis.
Sakamoto
T
T
Department of Dermatology, Hamamatsu University School of Medicine, Japan.
Nakayama
F
F
Tamamori
T
T
Takigawa
M
M
D000293:Adolescent; D000328:Adult; D000368:Aged; D000944:Antigens, Differentiation, B-Lymphocyte / Q000032:analysis*; D003876:Dermatitis, Atopic / Q000276:immunology*; D015232:Dinoprostone / Q000494:pharmacology; D005260:Female; D006801:Humans; D007370:Interferon Type I / Q000494:pharmacology; D007371:Interferon-gamma / Q000494:pharmacology; D007376:Interleukin-2 / Q000494:pharmacology; D015847:Interleukin-4 / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D010835:Phytohemagglutinins; D011961:Receptors, Fc / Q000032:analysis*; D017455:Receptors, IgE; D011994:Recombinant Proteins / Q000494:pharmacology; D016176:T-Lymphocyte Subsets / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*
D000944:Antigens, Differentiation, B-Lymphocyte; D007370:Interferon Type I; D007376:Interleukin-2; D010835:Phytohemagglutinins; D011961:Receptors, Fc; D017455:Receptors, IgE; D011994:Recombinant Proteins; D015847:Interleukin-4; D007371:Interferon-gamma; D015232:Dinoprostone