Supernatants from UVB radiation-exposed keratinocytes inhibit Langerhans cell presentation of tumor-associated antigens via IL-10 content.
Supernatants from UVB radiation-exposed keratinocytes inhibit Langerhans cell presentation of tumor-associated antigens via IL-10 content.
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来自 UVB 辐射暴露的角质形成细胞的上清液通过 IL-10 含量抑制朗格汉斯细胞呈递肿瘤相关抗原。
DOI：
10.1002/jlb.58.2.234
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发表时间：
1995
影响因子：
5.5
通讯作者：
Granstein,RD
中科院分区：
文献类型：
--
作者：
Beissert,S;Ullrich,SE;Hosoi,J;Granstein,RD
小鼠在体内暴露于中等范围的紫外线辐射（UVB）（280-320 mm）导致诱导迟发型超敏反应（DTH）的能力受到抑制。全身施用来自UVB暴露的角质形成细胞（KC）的上清液类似地抑制诱导DTH的能力，并且上清液中白细胞介素-10（IL-10）的存在已被证明是造成这种效果的原因。据推测，KC在体内暴露于UVB辐射后释放IL-10可能是UVB诱导的DTH抑制的原因，也可能是慢性UVB照射小鼠无法免疫排斥免疫原性UVB诱导的皮肤肿瘤的原因。为了直接检测UVB照射KC的上清液是否能抑制表皮朗格汉斯细胞（LC）对肿瘤相关抗原（TAA）的呈递，将转化的小鼠KC系PAM 212的培养物暴露于200 J/m2的UVB照射并获得24 h的上清液。将富含LC内容物的CAF 1（H-2a/d）表皮细胞（EC）暴露于来自照射（UV-SN）或模拟照射（MISN）PAM 212细胞的上清液3 h，然后在粒细胞-巨噬细胞集落刺激因子中培养16 h，然后用源自鼠梭形细胞肿瘤S1509 a（H-2a）的可溶性TAA脉冲。然后洗涤EC并以每周间隔皮下注射到幼稚CAF 1小鼠中三次用于引发。最后一次免疫后一周，用活S1509 a细胞皮下攻击这些小鼠，并随时间对肿瘤生长进行评分。用UV-SN预处理EC抑制了该免疫方案诱导的有效免疫。还用UV-SN或MI-SN处理EC 3小时，然后用TAA脉冲并注射到先前免疫的小鼠的后足垫中以引发DTH反应。用UV-SN预处理EC可抑制EC诱发DTH的能力，而MI-SN则无此作用。用IL-10的特异性中和抗体进行的中和研究表明，UV-SN中IL-10的存在抑制了诱导和激发免疫的抗原呈递。UV-SN通过IL-10的作用抑制表皮LC的肿瘤抗原呈递。58：234-240; 1995.
Exposure of mice to midrange UV radiation (UVB) (280–320 mm) in vivo leads to suppression of the ability to induce delayed-type hypersensitivity (DTH). Systemic administration of supernatants from UVB-exposed keratinocytes (KC) similarly inhibits the ability to induce DTH and the presence of interleukin-10 (IL-10) in the supernatants has been shown to be responsible for this effect. It has been hypothesized that release of IL-10 by KC after exposure to UVB radiation in vivo may be responsible for UVB-induced inhibition of DTH and alsp for the inability of chronically UVB-irradiated mice to immunologically reject immunogenic UVB-induced skin tumors. To test directly whether supernatants from UVB-irradiated KC can inhibit presentation of tumor-associated antigens (TAA) by epidermal Langerhans cells (LC), cultures of the transformed murine KC line PAM 212 were exposed to 200 J/m2of UVB radiation and 24 h supernatants obtained. CAF1(H-2a/d) epidermal cells (EC) enriched for LC content were exposed to supernatants from irradiated (UV-SN) or mock-irradiated (MISN) PAM 212 cells for 3 h followed by culture for 16 h in granulocyte-macrophage colony-stimulating factor and then were pulsed with soluble TAA derived from the murine spindle cell tumor S1509a (H-2a). ECs were then washed and injected subcutaneously into naive CAF1mice three times at weekly intervals for priming. One week after the final immunization these mice were challenged subcutaneously with live S1509a cells and tumor growth scored over time. Pretreatment of EC with UV-SN but not MI-SN inhibited the induction of effective immunity by this immunization scheme. ECs were also treated with UV-SN or MI-SN for 3 h then pulsed with TAA and injected into a hind footpad of previously immunized mice for elicitation of a DTH response. Pretreatment of EC with UV-SN but not MI-SN inhibited the ability of EC to elicit DTH. Neutralization studies with specific neutralizing antibodies to IL-10 demonstrated that the presence of IL-10 in UV-SN was responsible for the inhibition of antigen presentation both for induction and elicitation of immunity. UV-SN inhibits tumor antigen presentation by epidermal LC through the action of IL-10.J. Leukoc. Biol.58: 234–240; 1995.