Chen X J, Enerbäck L
Department of Pathology, Sahlgrenska Hospital, University of Göteborg, Sweden.
Immunology. 1994 Dec;83(4):595-600.
Athymic, nude (Lewis rnu/rnu) and normal (Lewis +/+) rats were used to study the T-cell dependence of the regulation of IgE receptors and IgE content on mast cells in vivo. We estimated the number of IgE receptors and the IgE content on peritoneal mast cells using a cytofluorometric technique. The secretory capacity of the mast cells was measured in terms of histamine release as a function of anti-IgE concentration by incubation with antibodies in vitro. Two groups of rats, aged 6 and 13 weeks, were examined. The mast cells of the rats belonging to the older age group (both normal and athymic) had a higher total protein (equivalent to dry mass or size) and mediator content (heparin, histamine and 5-hydroxytryptamine) in accordance with previous findings. Mast cells of the athymic rats of both age groups contained similar levels of IgE receptors and IgE and did not differ in these respects from those of the normal rats. Of the IgE receptors available for binding, about 80% were occupied by IgE in mast cells of normal and of athymic rats in both age groups. The anti-IgE-induced histamine release of the mast cells was, however, significantly lower in athymic rats compared to the normal controls. A change in housing from barrier-maintained to conventional conditions for 2 weeks enhanced the IgE-receptor and IgE content, as well as the releasability of histamine of the mast cells of both athymic and normal rats. The basal level of IgE occupancy of the receptors on mast cells was therefore not impaired in the athymic rats, as might be inferred from previous findings of a T-cell dependence of the IgE immune response. The results further indicate that T-lymphocyte-derived cytokines appear not to be required for either the expression of IgE receptors or for their ability to acquire IgE on mast cells, but such factors seem to enhance the release of histamine following the cross-linkage of the IgE receptor on mast cells in normal conditions.
无胸腺裸鼠（Lewis rnu/rnu）和正常大鼠（Lewis +/+）被用于研究体内肥大细胞上IgE受体调节和IgE含量的T细胞依赖性。我们使用细胞荧光测定技术估算了腹膜肥大细胞上IgE受体的数量和IgE含量。通过体外与抗体孵育，以组胺释放作为抗IgE浓度的函数来测量肥大细胞的分泌能力。对两组6周龄和13周龄的大鼠进行了检查。根据先前的研究结果，属于老年组的大鼠（正常和无胸腺）的肥大细胞具有更高的总蛋白（相当于干质量或大小）和介质含量（肝素、组胺和5-羟色胺）。两个年龄组的无胸腺大鼠的肥大细胞含有相似水平的IgE受体和IgE，在这些方面与正常大鼠没有差异。在正常和无胸腺大鼠的肥大细胞中，可用于结合的IgE受体约80%被IgE占据。然而，与正常对照组相比，无胸腺大鼠中肥大细胞的抗IgE诱导组胺释放显著降低。将饲养条件从屏障维持改为常规条件2周，增强了无胸腺和正常大鼠肥大细胞的IgE受体和IgE含量，以及组胺的释放能力。因此，肥大细胞上受体的IgE占据基础水平在无胸腺大鼠中并未受损，这与先前关于IgE免疫反应的T细胞依赖性的研究结果可能推断的情况不同。结果进一步表明，T淋巴细胞衍生的细胞因子似乎对于肥大细胞上IgE受体的表达或其获取IgE的能力并非必需，但在正常条件下，此类因子似乎会增强肥大细胞上IgE受体交联后组胺的释放。
