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正常人淋巴细胞产生的IgE由白细胞介素4诱导,而被γ干扰素、α干扰素和前列腺素E2抑制。

IgE production by normal human lymphocytes is induced by interleukin 4 and suppressed by interferons gamma and alpha and prostaglandin E2.

作者信息

Pène J, Rousset F, Brière F, Chrétien I, Bonnefoy J Y, Spits H, Yokota T, Arai N, Arai K, Banchereau J

机构信息

UNICET, Laboratory for Immunological Research, Dardilly, France.

出版信息

Proc Natl Acad Sci U S A. 1988 Sep;85(18):6880-4. doi: 10.1073/pnas.85.18.6880.

DOI:10.1073/pnas.85.18.6880
PMID:2970644
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC282082/
Abstract

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 on 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 portion 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.

摘要

研究了人重组白细胞介素4(IL-4)对富集B细胞的正常外周血单个核细胞抗体产生的影响。IL-4在体外优先诱导IgE合成。此外,观察到IgG产生有低水平诱导,而IL-4对IgA和IgM合成无影响。B细胞由IL-4诱导的IgE产生需要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,但它是IgE合成诱导的原因。干扰素γ(IFN-γ)、干扰素α(IFN-α)和前列腺素E2以剂量依赖方式阻断IL-4诱导的IgE产生。IFN-γ也抑制IL-4诱导的IgG产生。IFN-γ和IFN-α对IgE产生的这些抑制作用不能归因于毒性作用,因为IFN-α在IL-4存在下诱导IgM产生,而IFN-γ在抑制IL-2诱导的IgG产生方面无效。IFN-γ、IFN-α和前列腺素E2也抑制IL-4诱导的B细胞上IgE Fc段低亲和力受体(CD23)的表达,表明CD23表达与IL-4诱导的IgE产生之间存在关联。抗CD23单克隆抗体的F(ab')2片段抑制IL-4诱导的IgE产生这一发现支持了该理论。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f081/282082/3b8e3a5c70d4/pnas00297-0315-e.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f081/282082/0f2c60ffb457/pnas00297-0315-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f081/282082/edb2691c6232/pnas00297-0315-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f081/282082/dbbc7f5b4e34/pnas00297-0315-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f081/282082/8c597acd8c4d/pnas00297-0315-d.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f081/282082/3b8e3a5c70d4/pnas00297-0315-e.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f081/282082/0f2c60ffb457/pnas00297-0315-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f081/282082/edb2691c6232/pnas00297-0315-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f081/282082/dbbc7f5b4e34/pnas00297-0315-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f081/282082/8c597acd8c4d/pnas00297-0315-d.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f081/282082/3b8e3a5c70d4/pnas00297-0315-e.jpg

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