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Ultraviolet‐A1 (340–400 nm)‐mediated receptor and cytokine changes of transformed lymphocytes
Author(s) -
Godar Dianne E.,
Lucas Anne D.
Publication year - 2005
Publication title -
photodermatology, photoimmunology and photomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.736
H-Index - 60
eISSN - 1600-0781
pISSN - 0905-4383
DOI - 10.1111/j.1600-0781.2005.00133.x
Subject(s) - jurkat cells , apoptosis , il 2 receptor , receptor , cytokine , cd3 , biology , microbiology and biotechnology , flow cytometry , t cell receptor , fas ligand , foxp3 , cd19 , immunology , t cell , immune system , biochemistry , programmed cell death , cd8
Background: Ultraviolet‐A1 (340–400 nm) (UVA1) radiation causes singlet‐oxygen damage that depolarizes mitochondrial membranes triggering immediate apoptosis ( T ≤4 h), while it also causes oxidative damage to DNA inducing delayed apoptosis ( T ≥24 h). In this study, we examined some potential therapeutic endpoints associated with UVA1‐mediated immediate and delayed apoptosis, such as receptor and cytokine changes. Methods: We quantified the number of membrane‐bound CD3 receptors on transformed T lymphocytes (Jurkat) and the number of membrane‐bound CD19 receptors on transformed B lymphocytes (Daudi) using flow cytometry. We also quantified the release of the cytokines interferon γ (IFN‐γ) and interleukin‐2 (IL‐2) using enzyme‐linked immunosorbent assays. Results: Out of the entire population of cells, only the apoptotic Daudi cells immediately decreased CD19 expression via capping, while only the apoptotic Jurkat cells increased CD3 receptor expression 24 h post‐exposure. Both receptor changes occurred in a UVA1 dose‐dependent manner. We also examined other T‐cell receptors, such as CD4, CD25, and CD69, but they did not change for up to 24 h following exposure. During UVA1‐triggered immediate apoptosis of Jurkat T cells, IFN‐γ levels increased in a dose‐dependent manner at 4 h, but returned to baseline levels at 24 h post‐exposure, whereas, there was no significant change in IL‐2 at 4 or 24 h. Conclusion: Thus, UVA1‐triggered immediate apoptosis causes a rapid decrease in the number of CD19 receptors on Daudi B cells and release of IFN‐γ from Jurkat T cells at 4 h, and UVA1‐mediated delayed apoptosis causes an increase in the number of CD3 receptors on Jurkat T cells.