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.
复制标题
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
复制
发表时间:
1998
影响因子:
4.4
通讯作者:
I. Iwamoto
中科院分区:
文献类型:
--
作者:
A. Nakao;M. Kasai;K. Kumano;H. Nakajima;K. Kurasawa;I. Iwamoto
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.
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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)
影响因子:
--
作者:
Gregerson,DS;Obritsch,WF;Donoso,LA
通讯作者:
Donoso,LA
影响因子:
56.9
作者:
CHEN, YH;KUCHROO, VK;WEINER, HL
通讯作者:
WEINER, HL
DOI:
10.1073/pnas.91.14.6688
发表时间:
1994-07-05
影响因子:
11.1
作者:
FRIEDMAN, A;WEINER, HL
通讯作者:
WEINER, HL
DOI:
--
发表时间:
1991
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Scott,P
通讯作者:
Scott,P