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

BACKGROUND

Ultraviolet-A1 (340-400 nm) (UVA1) radiation causes singlet-oxygen damage that depolarizes mitochondrial membranes triggering immediate apoptosis (T < or = 4 h), while it also causes oxidative damage to DNA inducing delayed apoptosis (T > or = 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 gamma (IFN-gamma) 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-gamma 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-gamma 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.