Differential regulation of epidermal cell tumor-antigen presentation by IL-1alpha and IL-1beta.
Differential regulation of epidermal cell tumor-antigen presentation by IL-1alpha and IL-1beta.
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IL-1α 和 IL-1β 对表皮细胞肿瘤抗原呈递的差异调节。
DOI：
10.1046/j.1523-1747.1998.00291.x
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Granstein,RD
中科院分区：
文献类型：
--
作者：
Beissert,S;Hosoi,J;Stratigos,A;Brissette,J;Grabbe,S;Schwarz,T;Granstein,RD
IL-1以两种形式存在，称为IL-1α和IL-1β，它们在许多生物模型中发挥相似的作用。最近，有报道称这两种物种在某些系统中的活动存在一些差异。为了解决与朗格汉斯细胞有关的这个问题，在用S1509 a肿瘤相关抗原脉冲并随后用于对S1509 a的幼稚小鼠进行免疫之前，用IL-1α或IL-1β处理表皮细胞的朗格汉斯细胞富集制备物。虽然用100 U IL-1β/ml处理的表皮细胞能够诱导保护性肿瘤免疫（如对随后用活的S1509 a肿瘤细胞进行的肿瘤攻击的排斥所示），但用100 U IL-1α/ml处理的表皮细胞未能赋予保护性免疫。在1000 U/ml时，IL-1β还抑制表皮细胞诱导肿瘤免疫的能力。为了研究两种IL-1形式对引发肿瘤免疫的作用，通过s.c.注射死亡的S1509 a细胞。在肿瘤相关抗原脉冲之前，用100 U IL-1α或IL-1β/ml处理富集朗格汉斯细胞的表皮细胞。然后洗涤表皮细胞并注射到肿瘤免疫小鼠的后足垫中，并评估24小时足垫肿胀作为迟发型超敏反应的量度。暴露于IL-1α导致迟发型超敏反应的抑制，而IL-1β处理的表皮细胞引起正常（100 U/ml）或增强（1000 U/ml）水平的迟发型超敏反应。以往的实验表明，IL-1α对免疫诱导的抑制作用可能是由TNFα介导的。因此，评估了IL-1α或IL-1β诱导表皮细胞产生TNFα的能力。与IL-1β刺激相比，IL-1α诱导表皮细胞分泌显著更高量的TNFα蛋白。IL-1α和IL-1β似乎对表皮细胞抗原呈递能力有不同的调节作用。
IL-1 exists in two forms, termed IL-1α and IL-1β, which exert similar effects in a number of biologic models. Recently, there have been reports of some differences in the activities of these two species in some systems. To address this issue with regard to Langerhans cells, Langerhans cell-enriched preparations of epidermal cells were treated with either IL-1α or IL-1β before pulsing with S1509a tumor-associated antigens and subsequent use for immunization of naïve mice to S1509a. While epidermal cells treated with 100 U IL-1β per ml were able to induce protective tumor immunity (as indicated by the rejection of a subsequent tumor challenge with viable S1509a tumor cells), epidermal cells treated with 100 U IL-1α per ml failed to confer protective immunity. At 1000 U per ml, IL-1β also inhibited the ability of epidermal cells to induce tumor immunity. To investigate the effects of the two IL-1 forms on elicitation of tumor immunity, naïve mice were immunized against the S1509a tumor by s.c. injection of dead S1509a cells. Epidermal cells enriched for Langerhans cells were treated with either 100 U IL-1α or IL-1β per ml before tumor-associated antigens-pulsing. Epidermal cells were then washed and injected into a hind footpad of tumor immune mice and 24 h footpad swelling was assessed as a measure of delayed-type hypersensitivity. Exposure to IL-1α led to suppressed elicitation of delayed-type hypersensitivity, whereas IL-1β treated epidermal cells elicited a normal (100 U per ml) or enhanced (1000 U per ml) level of delayed-type hypersensitivity. Previous experiments indicated that the suppressive effects of IL-1α on induction of immunity may be mediated by TNFα. Therefore, the ability of IL-1α or IL-1β to induce epidermal cell production of TNFα was assessed. IL-1α induced epidermal cells to secrete significantly higher amounts of TNFα protein compared with stimulation with IL-1β. IL-1α and IL-1β appear to differentially regulate epidermal cell antigen presenting capability.