Ultraviolet-A1 (340–400 nm)-mediated receptor and cytokine changes of transformed lymphocytes

Authors


Corresponding author:
Dianne E. Godar, Ph.D.
Center for Devices and Radiological Health
Food and Drug Administration
9200 Corporate Blvd (HFZ-120)
Rockville, MD 20850
USA
Tel: +1 301 796-0299
Fax: +1 301 796-9826
e-mail: DEG@CDRH.FDA.GOV

Abstract

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.

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