CIS-UROCANIC ACID, A PRODUCT FORMED BY ULTRAVIOLET-B IRRADIATION OF THE SKIN, INITIATES AN ANTIGEN PRESENTATION DEFECT IN SPLENIC DENDRITIC CELLS INVIVO
CIS-UROCANIC ACID, A PRODUCT FORMED BY ULTRAVIOLET-B IRRADIATION OF THE SKIN, INITIATES AN ANTIGEN PRESENTATION DEFECT IN SPLENIC DENDRITIC CELLS INVIVO
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DOI：
10.1111/1523-1747.ep12462045
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发表时间：
1988-02-01
影响因子：
6.5
通讯作者：
MORRISON, H
中科院分区：
文献类型：
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作者：
NOONAN, FP;DEFABO, EC;MORRISON, H
尿刊酸（UCA，脱氨基组氨酸）是角质层的主要紫外线吸收成分。在紫外线照射下，天然存在的反式转化为顺式异构体。我们以前假设，紫外线诱导的全身抑制是由顺式UCA通过抗原呈递细胞缺陷的方式启动的。为了进一步验证这一假设，我们研究了脾树突状细胞（DC）的抗原呈递细胞（APC）功能。在1小时UV照射（27 kJ/m2）或静脉内施用50-200 μ g/小鼠的顺式或反式UCA后7天，从小鼠制备脾DC。来自UV照射或顺式UCA处理的小鼠的树突状细胞具有显著受损的（APC）能力，通过来自对DNP 6 OVA免疫的小鼠的纯化T细胞对用该抗原脉冲的DC的增殖反应来评估。trans-UCA诱导的小鼠树突状细胞具有正常的APC能力。来自所有四个处理组的DC中FcR+细胞的数量是相同的，并且来自UV照射或cis-UCA处理的小鼠的DC中IAd+细胞的数量和IAd表达的强度没有降低。来自UV或cis-UCA处理的小鼠的DC与来自正常小鼠的DC的混合物不抑制APC活性。UV或cis-UCA处理后3天的树突状细胞，与处理后7天的DC相比，具有正常的APC能力，表明APC缺陷产生的时间延迟。相反，将顺式-UCA或反式-UCA（66 μ g/ml）直接加入体外增殖测定中没有影响，表明顺式-UCA可以在体内活化。这些结果支持了我们最初的假设，即顺式UCA具有作为免疫功能调节剂的天然作用。
Urocanic acid (UCA, deaminated histidine) is a major ultraviolet-absorbing component of the stratum corneum. On UV irradiation, the naturally occurring trans form converts to the cis isomer. We have previously postulated that UV-induced systemic suppression is initiated by cis-UCA by way of an antigen-presenting cell defect. To test this hypothesis further, we have investigated the antigen-presenting cell (APC) function of splenic dendritic cells (DC). Splenic DC were prepared from mice 7 days after 1 h UV irrdiation (27 kJ/m2) or i.v. administration of 50-200 .mu.g/mouse of cis- or trans-UCA. Dendritic cells from UV-irradiated or cis-UCA-treated mice had a significantly impaired (APC) ability, assessed by the proliferative response of purified T cells from mice immune to DNP6 OVA to DC pulsed with this antigen. Dendritic cells from mice given trans-UCA had normal APC ability. The number of FcR+ cells was the same in DCs from all four treatment groups, and the number of IAd+ cells and the intensity of IAd expression were not decreased in DCs from UV-irradiated or cis-UCA-treated mice. Mixture of DCs from UV- or cis-UCA-treated mice with DCs from normal mice did not suppress APC activity. Dendritic cells taken 3 days after UV or cis-UCA treatment, in contrast to DC taken 7 days after treatment, had normal APC ability, indicating a time delay in the generation of the APC defect. In contrast, addition of cis-UCA or trans-UCA (66 .mu.g/ml)directly to an in vitro proliferation assay had no effect, suggesting that cis-UCA may be activted in vivo. These results support our original hypothesis that cis-UCA has a natural role as a modulator of immune function.