Phototherapy using ultraviolet B (UVB) has widely been used in the treatment of dermatologic diseases. Narrow-band UVB (NBUVB), which emits a concentrated UVB source of 311 nm, has been shown to have a profound therapeutic effect for the treatment of psoriasis.

The mechanism by which UVB treats clinical dermatoses is thought to be through the induction of apoptosis. Studies of broad-band UVB (BBUVB)- treated keratinocytes have demonstrated that apop- tosis is a direct consequence of dose and exposure time. NBUVB is also capable of inducing apop- tosis in keratinocytes, though at significantly higher doses of energy than BBUVB. NBUVB 1,000 mJ/cm2 induces apoptosis in approximately 50% of keratinocytes. This rate far exceeds the observed value of 1% for apoptosis in suprabasal keratinocytes under normal, physiological conditions.
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Transforming growth factor (TGF) is crucial for normal epidermal growth and differentiation. More than 30 members of the TGF- в family have been identified and grouped into several categories: pro- totypic TGF-в (TGF-в 1 to TGF^), bone mor- phogenetic proteins, growth/differentiation factors, and activins. The TGF name for this family of molecules is somewhat of a misnomer because TGF- 3 has antiproliferative effects on most cell types. The time course for growth arrest by UVB and TGF- в 1 are different: UVB-mediated growth arrest is known to occur within 3 hr after UVB irra­diation, while treatment with TGF- в 1 results in growth arrest in approximately 52 hr. In kerati- nocytes, secreted TGF- в 1 was downregulated less than 50% by UVA, while there was no significant alteration by UVB after irradiation with 20 and 40 J/cm2 and 10 and 20 mJ/cm2, respectively. The effect of TGF- в isoforms on keratinocytes during NBUVB irradiation at a dose that causes apoptosis has not been well-defined. In the present study, we investigate the differences in TGF- в isoform expre­ssion in keratinocytes after exposure to NBUVB.