PMID- 9114737
OWN - NLM
STAT- MEDLINE
DCOM- 19970528
LR  - 20201209
IS  - 0031-8655 (Print)
IS  - 0031-8655 (Linking)
VI  - 65
IP  - 4
DP  - 1997 Apr
TI  - 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.
PG  - 622-9
AB  - 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 narrow bandpass filter (335 +/- 5 nm full width at 
      half maximum), individuals were contact-sensitized with dinitrochlorobenzene 
      (DNCB) through a UVA II exposure site or through normal skin. UVA II induced a 
      marked decrease in the magnitude of skin immune responses (P < 0.0001). The UVA 
      II group had only 29% successful sensitizations, as compared to 83% in the 
      control group. The percentage of individuals who remained tolerant to DNCB after 
      two sensitizations was 23.6% for the UVA II-exposed group, as compared to 3.8% in 
      the controls (P = 0.006). UVA II also uniquely altered the type of 
      antigen-presenting cells present in the epidermis. Human leukocyte antigen 
      (HLA)-DR+ cells in control epidermal cell suspensions (C-EC) comprised a single, 
      homogeneous population of Langerhans cells (LC) with the phenotype: CD1ahi DRmid 
      CD11b CD36 (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 macrophage phenotype: CD1a- 
      DRhi CD11b+ CD36+ were increased in UVA II skin, relative to C-EC, these 
      comprised only 10.1 +/- 6.1% of the DR+ cells, which is less than that after UVB 
      exposure. Also distinct from UVB, a third population was found in UVA II-EC, 
      which exhibited a novel 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 ability to support 
      contact sensitization, induce active suppression (tolerance) and induce a 
      reduction in LC.
FAU - LeVee, G J
AU  - LeVee GJ
AD  - Department of Dermatology, University of Michigan, Ann Arbor, USA.
FAU - Oberhelman, L
AU  - Oberhelman L
FAU - Anderson, T
AU  - Anderson T
FAU - Koren, H
AU  - Koren H
FAU - Cooper, K D
AU  - Cooper KD
LA  - eng
PT  - Congress
PL  - United States
TA  - Photochem Photobiol
JT  - Photochemistry and photobiology
JID - 0376425
RN  - 0 (Dinitrochlorobenzene)
RN  - 0 (HLA-DR Antigens)
SB  - IM
MH  - Adaptation, Physiological/*radiation effects
MH  - Antigen-Presenting Cells/*radiation effects
MH  - Dinitrochlorobenzene/administration & dosage/pharmacology
MH  - Epidermis/immunology/physiology/*radiation effects
MH  - HLA-DR Antigens/immunology
MH  - Humans
MH  - Immunization
MH  - Skin/immunology/*radiation effects
MH  - Skin Physiological Phenomena
MH  - *Ultraviolet Rays
EDAT- 1997/04/01 00:00
MHDA- 1997/04/01 00:01
CRDT- 1997/04/01 00:00
PHST- 1997/04/01 00:00 [pubmed]
PHST- 1997/04/01 00:01 [medline]
PHST- 1997/04/01 00:00 [entrez]
AID - 10.1111/j.1751-1097.1997.tb01903.x [doi]
PST - ppublish
SO  - Photochem Photobiol. 1997 Apr;65(4):622-9. doi: 
      10.1111/j.1751-1097.1997.tb01903.x.