High-dose oral tolerance prevents antigen-induced eosinophil recruitment into the mouse airways.

High-dose oral tolerance prevents antigen-induced eosinophil recruitment into the mouse airways.
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高剂量口服耐受可防止抗原诱导的嗜酸性粒细胞募集到小鼠气道中。

DOI:
10.1093/intimm/10.4.387
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发表时间:
1998
影响因子:
4.4
通讯作者:
I. Iwamoto
I. Iwamoto
中科院分区:
医学3区
文献类型:
--
作者:
A. Nakao;M. Kasai;K. Kumano;H. Nakajima;K. Kurasawa;I. Iwamoto

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我们之前已经证明抗原诱导的嗜酸性粒细胞募集到致敏小鼠的组织中是由CD4+ T细胞和IL-5介导的。为了确定口服耐受诱导是否下调抗原诱导的嗜酸性粒细胞向组织募集,我们研究了口服一种蛋白抗原对致敏小鼠气管中抗原诱导的嗜酸性粒细胞浸润、对气道中抗原诱导的CD4+ T细胞浸润和IL-5产生的影响,以及对小鼠脾细胞中IL-2、IL-4、IL-5和ifn - γ体外产生的影响。高剂量口服一种蛋白抗原可抑制抗原诱导的气管嗜酸性粒细胞浸润和小鼠体内抗原特异性的IgE抗体产生。口服抗原也抑制了吸入抗原后小鼠支气管肺泡灌洗液中CD4+ T细胞向气管的募集和IL-5水平。在体外抗原诱导的小鼠脾脏细胞中IL-2、ifn - γ、IL-4和IL-5的产生减少,表明在体内诱导了Th1和Th2细胞耐受。另一方面,抗原免疫时预处理抗转化生长因子- β抗体对抗原喂养小鼠抗原诱导的嗜酸性粒细胞募集和IgE抗体产生的抑制作用无显著影响。最后,通过FACS分析,抗原喂养后TCR转基因小鼠的抗原特异性CD4+ T细胞未被删除。综上所述,这些结果表明,大剂量口服耐受在体内不仅诱导Th1细胞耐受,而且诱导Th2细胞耐受,从而抑制抗原诱导的嗜酸性粒细胞向组织募集。
We have previously shown that antigen-induced eosinophil recruitment into the tissue of sensitized mice is mediated by CD4+ T cells and IL-5. To determine whether the induction of oral tolerance down-regulates antigen-induced eosinophil recruitment into the tissue, we studied the effect of oral administration of a protein antigen on antigen-induced eosinophil infiltration in the trachea of sensitized mice, on antigen-induced CD4+ T cell infiltration and IL-5 production in the airways, and on the in vitro production of IL-2, IL-4, IL-5 and IFN-gamma in spleen cells of the mice. Oral administration of a protein antigen in high doses inhibited antigen-induced eosinophil infiltration in the trachea and IgE antibody production in mice in an antigen-specific manner. The oral administration of antigen also suppressed both CD4+ T cell recruitment into the trachea and IL-5 levels in the bronchoalveolar lavage fluids of the mice after antigen inhalation. In vitro antigen-induced production of IL-2, IFN-gamma, IL-4 and IL-5 was decreased in spleen cells of antigen-fed mice, indicating the induction of both Th1 and Th2 cell tolerance in vivo. On the other hand, pretreatment with anti-transforming growth factor-beta antibody at the time of immunization with antigen had no significant effect on the inhibition of antigen-induced eosinophil recruitment and IgE antibody production in antigen-fed mice. Finally, antigen-specific CD4+ T cells were not deleted in TCR transgenic mice after antigen feeding by FACS analysis. Taken together, these results indicate that high-dose oral tolerance induces not only Th1 but also Th2 cell tolerance in vivo and thereby inhibits antigen-induced eosinophil recruitment into the tissue.
DOI: 10.1164/arrd.1987.135.2.433
发表时间: 1987
期刊: The American review of respiratory disease
影响因子: --
作者:
Metzger,WJ;Zavala,D;Richerson,HB;Moseley,P;Iwamota,P;Monick,M;Sjoerdsma,K;Hunninghake,GW
通讯作者: Hunninghake,GW
DOI: --
发表时间: 1993
期刊: Journal of immunology (Baltimore, Md. : 1950)
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DOI: 10.1126/science.7520605
发表时间: 1994-08-26
期刊: SCIENCE
影响因子: 56.9
作者:
CHEN, YH;KUCHROO, VK;WEINER, HL
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DOI: 10.1073/pnas.91.14.6688
发表时间: 1994-07-05
影响因子: 11.1
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通讯作者: WEINER, HL
IFN-gamma 调节皮肤利什曼病小鼠模型中 Th1 和 Th2 反应的早期发展。
DOI: --
发表时间: 1991
期刊: Journal of immunology (Baltimore, Md. : 1950)
影响因子: --
作者:
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通讯作者: Scott,P