IL-3 is required for increases in blood basophils in nematode infection in mice and can enhance IgE-dependent IL-4 production by basophils in vitro.

IL-3 is required for increases in blood basophils in nematode infection in mice and can enhance IgE-dependent IL-4 production by basophils in vitro.
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DOI:
10.1038/labinvest.2008.88
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发表时间:
2008-11
期刊:
Laboratory investigation; a journal of technical methods and pathology
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其他
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在巴西尼波圆线虫(Nippostrongylus brasiliensis, n.b.)感染引起的免疫反应中,以及在其他情况下,嗜碱性细胞代表潜在的效应细胞和免疫调节细胞,以及IL-4的潜在来源。然而,调节小鼠血液中嗜碱性细胞数量的因素,或这些细胞产生IL-4的能力,尚不完全清楚。我们发现,感染N.b.线虫或委内瑞拉圆形线虫(s.v.)的小鼠,血液嗜碱性粒细胞的数量大幅增加(高达循环血液白细胞的18%)。在IL-3−/−vs IL-3+/+小鼠以及IL-3处理的IL-3−/−小鼠中进行的实验表明,在N.b.或S.v.感染期间,血液或骨髓嗜碱性粒细胞的增加基本上都依赖于IL-3。IL-3−/−或IL-3+/+小鼠的许多血液、骨髓或肝脏来源的嗜碱性粒细胞在体外抗ige刺激下表达细胞内IL-4。然而,在体外用外源性IgE孵育细胞后,来自IL-3+/+小鼠的血液或肝脏来源的嗜碱性粒细胞在抗IgE刺激下表现出比来自IL-3−/−小鼠的嗜碱性粒细胞更高的细胞内IL-4水平。因此,IL-3是在N.b.或S.v.感染小鼠期间观察到的血液嗜碱性粒细胞水平显著增加的主要调节因子,并且在体外抗ige激活嗜碱性粒细胞后也可以提高细胞内IL-4水平。
Basophils represent potential effector and immunoregulatory cells, as well as a potential source of IL-4, during the immune response elicited by infection with the nematode Nippostrongylus brasiliensis (N.b.), and in other settings. However, the factors which regulate the numbers of blood basophils in mice, or the ability of these cells to produce IL-4, are not fully understood. We found that infection of mice with the nematodes N.b. or Strongyloides venezuelensis (S.v.) induced substantial increases in the numbers of blood basophils (to as high as 18 % of circulating blood leukocytes). Experiments in IL-3−/− vs IL-3+/+ mice, and in IL-3-treated IL-3−/− mice, showed that essentially all of the increases in blood or bone marrow basophils during N.b. or S.v. infection were IL-3-dependent. Many of the blood, bone marrow or liver-derived basophils from IL-3−/− or IL-3+/+ mice expressed intra-cellular IL-4 upon stimulation with anti-IgE in vitro. However, after incubation of the cells with exogenous IgE in vitro, blood- or liver-derived basophils from IL-3+/+ mice exhibited higher levels of intra-cellular IL-4 after stimulation with anti-IgE than did basophils derived from IL-3−/− mice. Thus, IL-3 is a major regulator of the marked increases in blood basophil levels observed during infection of mice with N.b. or S.v. and also can enhance levels of intra-cellular IL-4 upon activation of basophils with anti-IgE in vitro.
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