Interleukin production by neonatal spleen cells during and as a result of antigen presentation: the effect of ultraviolet light.

Lymphokine research Pub Date : 1989-01-01
D Levin, H Gershon
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Abstract

Antigen presentation by neonatal murine spleen cells and the production of lymphokines and interleukins involved in the stimulation of a T-helper-2 (TH2) cell line (D10-G4.1) were studied as were the effects of ultra violet (UV)-irradiation on this system. Neonatal spleen cells are less capable than adult cells of performing the initial steps of the immune response required for antigen dependent activation of TH2 cells. These steps include soluble antigen processing and presentation and as a result reduced production of IL-4 and IL-1-Inducer Factor ("IL-1-IF") by the T-helper cells and reduced production of IL-1 and IL-2 by the antigen presenting cell population. Spontaneous membrane IL-1 activity is low in the neonate, however, when exposed to "IL-1-IF" they can express adult levels. Ultra-violet (UV) irradiation of the antigen presenting population has a damaging effect on all the above mentioned processes. Antigen processing and presentation, induction of D10 IL-4 production and proliferation, and IL-2 production demonstrate two different age related patterns of UV-irradiation induced damage: a dose dependent inhibition when adult cells are irradiated and an inverse effect in which low doses of irradiation were more inhibitory than higher doses when neonatal cells are irradiated. However, the secretion and membrane expression of IL-1 by both age groups are directly and totally inhibited by the range of UV-irradiation doses used and cannot be reinduced with a supplement of a crude "IL-1-IF". While the capacity to produced IL-1 is totally destroyed by UV-irradiation, the ability to produce IL-2 remains intact and remains responsive to an "IL-2-Inducer" activity during proper antigen presentation. The low responses of neonatal antigen presenting spleen cell populations and the damaging effect of UV on both neonatal and adult responses are not due to the induction of suppressor factors.

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新生儿脾细胞在抗原呈递期间及其结果产生白细胞介素:紫外线的影响。
本文研究了新生鼠脾细胞抗原呈递和淋巴因子和白细胞介素的产生,这些因子参与刺激t -辅助性2 (TH2)细胞系(D10-G4.1),并研究了紫外线(UV)照射对该系统的影响。新生儿脾细胞比成人细胞执行抗原依赖性激活TH2细胞所需的免疫反应的初始步骤的能力更弱。这些步骤包括可溶性抗原的处理和提呈,结果减少了t辅助细胞产生的IL-4和IL-1诱导因子(“IL-1- if”),减少了抗原提呈细胞群产生的IL-1和IL-2。自发膜IL-1活性在新生儿中较低,然而,当暴露于“IL-1- if”时,它们可以表达成人水平。抗原呈递群体的紫外线照射对上述所有过程都有破坏作用。抗原加工和提呈,诱导D10 - IL-4的产生和增殖,以及IL-2的产生显示了两种不同的年龄相关的紫外线照射诱导损伤模式:成年细胞受照射时的剂量依赖性抑制,以及新生儿细胞受照射时低剂量的抑制比高剂量的抑制更强的反向效应。然而,两个年龄组的IL-1的分泌和膜表达直接和完全受到所使用的紫外线照射剂量范围的抑制,并且不能通过补充粗“IL-1- if”来重新诱导。虽然产生IL-1的能力完全被紫外线照射破坏,但产生IL-2的能力保持不变,并在适当的抗原呈递过程中对“IL-2诱导剂”活性保持反应。新生儿抗原呈递脾脏细胞群的低反应和紫外线对新生儿和成人反应的破坏作用不是由于抑制因子的诱导。
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