Title of article :
UVA1 radiation (340–400 nm) interferes with the perforin-granule system of CD8hi+ cytotoxic T lymphocytes in vitro
Author/Authors :
Ambach، نويسنده , , Andreas and Bonnekoh، نويسنده , , Bernd and Gollnick، نويسنده , , Harald، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2006
Pages :
8
From page :
236
To page :
243
Abstract :
UVA1-irradiation was introduced as an innovative and effective phototherapy of atopic dermatitis (AD) and other skin diseases. In AD, a defect of a central apoptosis inducing effector system involved in immunoregulation and immune defense, i.e., the system of perforin-granules in cytotoxic T lymphocytes (CTL), was recently reported: perforin-reduction and perforin-hyperreleasability. We now investigated UVA1-effects on the perforin-granule system in vitro. Peripheral blood CTLs were exposed in vitro to 10–100 J/cm2 UVA1 (340–400 nm), and to 30–150 mJ/cm2 UVB (280–315 nm) as a control. A time-dependent perforin-granule release was induced by phorbol 12-myristate 13-acetate (PMA) and ionomycin. This release was inhibited dose-dependently by UVA1, but not by UVB. An UVA1-dose dependent pattern of sensitive (80%) and insensitive (20%) individuals was found. The kinetics of perforin release in AD-CTLs, i.e. hyperreleasability, was normalized by 50 J/cm2 UVA1 in vitro. Sodium azide as a quencher of reactive oxygen species prevented the UVA1-mediated inhibition of perforin-granule release. Our data demonstrate for the first time a dose- and wavelength-dependent UVA1-effect in vitro on a major effector system of cytotoxic lymphocytes, the system of perforin-granules. This might contribute to the further understanding of immunomodulatory UVA1-effects in vivo.
Keywords :
cytotoxicity , skin , Regulatory T cells , ultraviolet light , Phototherapy , Atopic eczema dermatitis syndrome
Journal title :
Journal of Photochemistry and Photobiology B:Biology
Serial Year :
2006
Journal title :
Journal of Photochemistry and Photobiology B:Biology
Record number :
1875366
Link To Document :
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