人类皮肤暴露于UVA II会导致免疫能力下降、耐受性诱导增加以及表皮抗原呈递细胞改变的独特模式。

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.

作者信息

LeVee G J, Oberhelman L, Anderson T, Koren H, Cooper K D

机构信息

Department of Dermatology, University of Michigan, Ann Arbor, USA.

出版信息

Photochem Photobiol. 1997 Apr;65(4):622-9. doi: 10.1111/j.1751-1097.1997.tb01903.x.

DOI:10.1111/j.1751-1097.1997.tb01903.x

PMID:9114737

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 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.

摘要

人们对增加暴露于UVA II（320 - 340纳米）（即在使用防晒霜和长时间户外暴露、日光浴沙龙期间）所带来的风险了解不足。因此，我们探究了UVA II对人体皮肤免疫反应的影响。使用一个用窄带通滤光片（半高全宽为335±5纳米）过滤的氙弧灯进行单次局部照射（4个最小红斑剂量[MED]）后，通过UVA II照射部位或正常皮肤对个体进行二硝基氯苯（DNCB）接触致敏。UVA II导致皮肤免疫反应的强度显著降低（P < 0.0001）。UVA II组的致敏成功率仅为29%，而对照组为83%。在两次致敏后仍对DNCB耐受的个体百分比，UVA II照射组为23.6%，而对照组为3.8%（P = 0.006）。UVA II还独特地改变了表皮中存在的抗原呈递细胞的类型。对照表皮细胞悬液（C - EC）中的人类白细胞抗原（HLA） - DR +细胞由单一的、表型均一的朗格汉斯细胞（LC）群体组成：CD1ahi DRmid CD11b CD36（占EC的1.5±0.3%）。UVA II照射使此类LC的数量减少至EC的0.6±0.2%。尽管相对于C - EC，表达巨噬细胞表型：CD1a - DRhi CD11b + CD36 +的细胞在UVA II照射的皮肤中有所增加，但这些细胞仅占DR +细胞的10.1±6.1%，低于UVB照射后。与UVB也不同的是，在UVA II - EC中发现了第三种细胞群体，其表现出一种新的表型：CD1a + DR + CD36 + CD11b +；这些细胞占DR + UVA II - EC的11.1±6.9%。总之，尽管在浸润的DR +细胞方面存在上述差异，但UVB和UVA II均会降低皮肤支持接触致敏的能力、诱导主动抑制（耐受）并导致LC数量减少。