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感染巴西日圆线虫或注射抗IgD抗体可显著增强非B、非T细胞通过Fc受体介导的白细胞介素4的产生。

Infection with Nippostrongylus brasiliensis or injection of anti-IgD antibodies markedly enhances Fc-receptor-mediated interleukin 4 production by non-B, non-T cells.

作者信息

Conrad D H, Ben-Sasson S Z, Le Gros G, Finkelman F D, Paul W E

机构信息

Department of Microbiology and Immunology, Medical College of Virginia, Richmond 23298.

出版信息

J Exp Med. 1990 May 1;171(5):1497-508. doi: 10.1084/jem.171.5.1497.

Abstract

Non-B, non-T cells from spleen and bone marrow of naive mice produce IL-4 upon stimulation by plate-bound IgE or IgG2a in the presence of IL-3. Infection of mice with Nippostrongylus brasiliensis (Nb) or injection of anti-IgD antibodies, treatments known to cause striking polyclonal IgE responses, increase the number of splenic non-B, non-T cells and cause 10-30-fold increase in IL-4 production by a standard number of these cells. In Nb-infected mice, IL-4 producing non-B, non-T cells can be found in the lungs, a site through which Nb larvae migrate. Non-B, non-T cells from anti-IgD-injected mice produce IL-4 in response to anti-IgE antibodies, indicating that these cells have been sensitized in vivo with IgE and that crosslinkage of such IgE can lead to stimulation of lymphokine production. Similarly, non-B, non-T cells from Nb-infected mice produce IL-4 upon stimulation with Nb-antigen, indicating that antigen can also crosslink receptors on in vivo sensitized non-B, non-T cells and stimulate lymphokine production. The striking increases in the IL-4-producing capacity of the splenic non-B, non-T cell population in anti-IgD-injected and Nb-infected mice and the in vivo sensitization of these cells strongly suggests that they may have an important role in lymphokine production in helminthic infections and other situations marked by striking elevations of serum IgE levels.

摘要

未接触过抗原的小鼠脾脏和骨髓中的非B、非T细胞,在IL-3存在的情况下,受到板结合型IgE或IgG2a刺激后会产生IL-4。用巴西日圆线虫(Nb)感染小鼠或注射抗IgD抗体(已知会引起显著多克隆IgE反应的处理方法),会增加脾脏中非B、非T细胞的数量,并使这些细胞的标准数量产生的IL-4增加10到30倍。在感染Nb的小鼠中,产生IL-4的非B、非T细胞可在肺部发现,Nb幼虫会通过该部位迁移。注射抗IgD小鼠的非B、非T细胞会对抗IgE抗体产生反应而产生IL-4,这表明这些细胞已在体内被IgE致敏,且这种IgE的交联可导致淋巴因子产生的刺激。同样,感染Nb小鼠的非B、非T细胞在用Nb抗原刺激后会产生IL-4,这表明抗原也可交联体内致敏的非B、非T细胞上的受体并刺激淋巴因子产生。注射抗IgD和感染Nb的小鼠脾脏非B、非T细胞群体产生IL-4的能力显著增加,以及这些细胞在体内的致敏,强烈表明它们可能在蠕虫感染和其他血清IgE水平显著升高的情况下的淋巴因子产生中发挥重要作用。

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