IGE PRODUCTION BY NORMAL HUMAN-LYMPHOCYTES IS INDUCED BY INTERLEUKIN-4 AND SUPPRESSED BY INTERFERON-GAMMA AND INTERFERON-ALPHA AND PROSTAGLANDIN-E2

IGE PRODUCTION BY NORMAL HUMAN-LYMPHOCYTES IS INDUCED BY INTERLEUKIN-4 AND SUPPRESSED BY INTERFERON-GAMMA AND INTERFERON-ALPHA AND PROSTAGLANDIN-E2
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DOI:
10.1073/pnas.85.18.6880
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发表时间:
1988-09-01
影响因子:
11.1
通讯作者:
DEVRIES, JE
DEVRIES, JE
中科院分区:
综合性期刊1区
文献类型:
--
作者:
PENE, J;ROUSSET, F;DEVRIES, JE

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研究了人重组白细胞介素4 (IL-4)对正常外周血单个核细胞产生抗体的影响。IL-4优先诱导体外IgE合成。此外,观察到低诱导IgG的产生,而IL-4对IgA和IgM的合成没有影响。IL-4诱导的B细胞产生IgE需要T细胞和单核细胞,但被抗IL-4抗血清特异性抑制,这表明尽管IL-4间接起作用,但它负责诱导IgE合成。干扰素阻断il -4诱导的IgE产生呈剂量依赖性。(IFN- γ),干扰素。(IFN- α)和前列腺素E2。干扰素可以利用。也能抑制il -4诱导的IgG产生。这些IFN- γ的抑制作用。和干扰素-.alpha。IgE的产生不能归因于毒性作用,因为IFN-。在IL-4存在的情况下诱导IgM的产生,而IFN-。对IL-2、IFN- γ诱导的IgG产生无抑制作用。干扰素-.alpha。前列腺素E2也能抑制il -4诱导的低亲和受体(CD23)在B细胞上的表达,表明CD23的表达与il -4诱导的IgE产生之间存在关联。这一理论得到了il -4诱导的IgE产生被抗cd23单克隆抗体F (ab ")2片段抑制的发现的支持。
The effect of human recombinant interleukin 4 (IL-4) on antibody production by normal peripheral blood mononuclear cells enriched for B cells was investigated. IL-4 preferentially induced IgE synthesis in vitro. In addition, a low induction of IgG production was observed, whereas IL-4 had no effect on IgA and IgM synthesis. The IL-4-induced IgE production by B cells required T cells and monocytes but was specifically inhibited by an anti-IL-4 antiserum indicating that, although IL-4 acts indirectly, it is responsible for the induction of IgE synthesis. IL-4-induced IgE production was blocked in a dose-dependent way by interferon .gamma. (IFN-.gamma.), interferon .alpha. (IFN-.alpha.), and prostaglandin E2. IFN-.gamma. also inhibited IL-4-induced IgG production. These inhibitory effects of IFN-.gamma. and IFN-.alpha. an IgE production cannot be attributed to toxic effects since IFN-.alpha. induced IgM production in the presence of IL-4, whereas IFN-.gamma. was ineffective in inhibiting IgG production induced by IL-2, IFN-.gamma., IFN-.alpha., and prostaglandin E2 also inhibited IL-4-induced expression of the low-affinity receptor for the Fc production of IgE (CD23) on B cells, indicating that there is an association between CD23 expression and IL-4-induced IgE production. This theory was supported by the finding that IL-4-induced IgE production was inhibited by F (ab'')2 fragments of an anti-CD23 monoclonal antibody.