Fcε receptor II/CD23+ lymphocytes in atopic dermatitis. III. Aberrant control in the in vitro expression of FcεRII/CD23 on peripheral blood T cells in atopic dermatitis
SUMMARY In vitro FcεRII 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 we...
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| Published in | Clinical and experimental immunology Vol. 87; no. 1; pp. 87 - 93 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford, UK
Blackwell Publishing Ltd
01.01.1992
Blackwell |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0009-9104 1365-2249 |
| DOI | 10.1111/j.1365-2249.1992.tb06418.x |
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| Abstract | SUMMARY
In vitro FcεRII 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 FcεRII and to lymphoid cell‐surface antigens and analysed by flow cytometry, rIL‐4, but not rIL‐2, specifically induced FcεRII 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 FcεRII+ T cells (Tε cells), whereas the frequency of B cells bearing FcεRII(Bε cells) was significantly higher in patients with extensive atopic dermatitis than in those with mild atopic dermatitis and other subjects. Comparable levels of Tε 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 Tε cell populations induced specifically by rIL‐4, PHA and PHA plus rIL‐2, patients with atopic dermatitis had a greater tendency for FcεRII expression on CD8+ T cells compared with patients with eczematous dermatitis and normal individuals. Recombinant interferon‐gamma (rIFN‐γ), but not rIFN‐α or prostaglandin E2 (PGE2), suppressed the generation of Tε cells by rIL‐4 in atopics and non‐atopics to the same degree. These results suggest the aberrant control of FcεRII expression on T cells, especially those bearing CD8, in atopic dermatitis. |
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| AbstractList | SUMMARY
In vitro FcεRII 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 FcεRII and to lymphoid cell‐surface antigens and analysed by flow cytometry, rIL‐4, but not rIL‐2, specifically induced FcεRII 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 FcεRII+ T cells (Tε cells), whereas the frequency of B cells bearing FcεRII(Bε cells) was significantly higher in patients with extensive atopic dermatitis than in those with mild atopic dermatitis and other subjects. Comparable levels of Tε 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 Tε cell populations induced specifically by rIL‐4, PHA and PHA plus rIL‐2, patients with atopic dermatitis had a greater tendency for FcεRII expression on CD8+ T cells compared with patients with eczematous dermatitis and normal individuals. Recombinant interferon‐gamma (rIFN‐γ), but not rIFN‐α or prostaglandin E2 (PGE2), suppressed the generation of Tε cells by rIL‐4 in atopics and non‐atopics to the same degree. These results suggest the aberrant control of FcεRII expression on T cells, especially those bearing CD8, 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. In vitro FcεRII 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 FcεRII and to lymphoid cell-surface antigens and analysed by flow cytometry, rIL-4, but not rIL-2, specifically induced FcεRII 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 FcεRII+ T cells (Tε cells), whereas the frequency of B cells bearing FcεRII(Bε cells) was significantly higher in patients with extensive atopic dermatitis than in those with mild atopic dermatitis and other subjects. Comparable levels of Tε 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 Tε cell populations induced specifically by rIL-4, PHA and PHA plus rIL-2, patients with atopic dermatitis had a greater tendency for FcεRII expression on CD8+ T cells compared with patients with eczematous dermatitis and normal individuals. Recombinant interferon-gamma (rIFN-γ), but not rIFN-α or prostaglandin E2 (PGE2), suppressed the generation of Tε cells by rIL-4 in atopics and non-atopics to the same degree. These results suggest the aberrant control of FcεRII expression on T cells, especially those bearing CD8, 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.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. |
| Author | NAKAYAMA, F. TAMAMORI, T. SAKAMOTO, T. TAKIGAWA, M. |
| AuthorAffiliation | Department of Dermatology, Hamamatsu University School of Medicine, Japan |
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| Keywords | Human Immunopathology Skin disease Regulation(control) Fc-Fragment Atopic dermatitis T-Lymphocyte Biosynthesis Cell subpopulation Cell surface Biological receptor |
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In vitro FcεRII expression was examined in patients with atopic dermatitis, those with non‐atopic eczematous dermatitis and normal individuals... In vitro FcεRII expression was examined in patients with atopic dermatitis, those with non-atopic eczematous dermatitis and normal individuals following... In vitro Fc epsilon RII expression was examined in patients with atopic dermatitis, those with non-atopic eczematous dermatitis and normal individuals... |
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| SubjectTerms | Adolescent Adult Aged Antigens, Differentiation, B-Lymphocyte - analysis atopic dermatitis Biological and medical sciences cells Dermatitis, Atopic - immunology Dermatology Dinoprostone - pharmacology FcεRII IL‐4 Female Humans in vitro culture Interferon Type I - pharmacology Interferon-gamma - pharmacology Interleukin-2 - pharmacology Interleukin-4 - pharmacology Male Medical sciences Middle Aged Phytohemagglutinins Receptors, Fc - analysis Receptors, IgE Recombinant Proteins - pharmacology Skin involvement in other diseases. Miscellaneous. General aspects T-Lymphocyte Subsets - immunology T-Lymphocytes - immunology |
| Title | Fcε receptor II/CD23+ lymphocytes in atopic dermatitis. III. Aberrant control in the in vitro expression of FcεRII/CD23 on peripheral blood T cells in atopic dermatitis |
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