UVA-II EXPOSURE OF HUMAN SKIN RESULTS IN DECREASED IMMUNIZATION CAPACITY, INCREASED INDUCTION OF TOLERANCE AND A UNIQUE PATTERN OF EPIDERMAL ANTIGEN-PRESENTING CELL ALTERATION

Citation
Gj. Levee et al., UVA-II EXPOSURE OF HUMAN SKIN RESULTS IN DECREASED IMMUNIZATION CAPACITY, INCREASED INDUCTION OF TOLERANCE AND A UNIQUE PATTERN OF EPIDERMAL ANTIGEN-PRESENTING CELL ALTERATION, Photochemistry and photobiology, 65(4), 1997, pp. 622-629
Citations number
61
Categorie Soggetti
Biophysics,Biology
ISSN journal
00318655
Volume
65
Issue
4
Year of publication
1997
Pages
622 - 629
Database
ISI
SICI code
0031-8655(1997)65:4<622:UEOHSR>2.0.ZU;2-O
Abstract
The risks incurred from increased exposure to UVA II (320-340 nm) (i.e . during sunscreen use and extended outdoor exposure, tanning parlors) are not well understood. Therefore, we explored the effects of UVA II on skin immune responses in humans. After a single local exposure (4 minimum erythemal dose [MED]) using a xenon are lamp filtered with a n arrow bandpass filter (335 +/- 5 nm full width at half maximum), indiv iduals were contact-sensitized with dinitrochlorobenzene (DNCB) throug h a UVA II exposure site or through normal skin, UVA II induced a mark ed decrease in the magnitude of skin immune responses (P < 0.0001). Th e UVA II group had only 29% successful sensitizations, as compared to 83% in the control group. The percentage of individuals who remained t olerant to DNCB after two sensitizations was 23.6% for the UVA II-expo sed group, as compared to 3.8% in the controls (P = 0.006). UVA II als o uniquely altered the type of antigen-presenting cells present in the epidermis. Human leukocyte antigen (HLA)-DR+ cells in control epiderm al cell suspensions (C-EC) comprised a single, homogeneous population of Langerhans cells (LC) with the phenotype: CD1a(hi) DRmid CD11b(-) C D36(-) (1.5 +/- 0.3% of EC). UVA II irradiation reduced the number of such LC to 0.6 +/- 0.2% of EC. Although cells expressing the macrophag e phenotype: CD1a(-) DRhi CD(11)b(+) CD36(+) were increased in UVA II skin, relative to C-EC, these comprised only 10.1 +/- 6.1% of the DRcells, which is less than that after UVB exposure. Also distinct from UVB, a third population was found in UVA II-EC, which exhibited a nove l phenotype: CD1a(+) DR+ CD36(+) CD11b(+); these comprised 11.1 +/- 6. 9% of the DR+ UVA II-EC. In conclusion, despite the above differences in infiltrating DR+ cells, both UVB and UVA II reduce the skin's abili ty to support contact sensitization, induce active suppression (tolera nce) and induce a reduction in LC.