Two faces of IgE-mediated allergic reactions.

我们测试了IgE交联刺激可能通过矛盾效应作用于携带fc - ri的细胞的可能性：即激活与抑制激活。使用人类嗜碱性细胞，我们发现ige介导的弱刺激持续诱导对随后的ige介导的强刺激的嗜碱性细胞释放性的深刻抑制。细胞内酪氨酸激酶、Lyn、Syk和Btk的半定量采用细胞内FACS分析；然而，这些激酶的数量，如其荧光强度所示，与未处理的细胞相比，在处理过的细胞中没有变化。有趣的是，IgE和抗IgE的微妙平衡在调节细胞释放的命运中很重要；当抗IgE抗体过多时，嗜碱性细胞立即被激活，但当IgE和抗IgE抗体平衡时，细胞失去释放性而不释放颗粒内容物（表现为脱敏）。这些结果表明，ige介导的对携带fcε ri细胞的影响不仅仅是细胞刺激；IgE可介导以下IgE介导的细胞反应的复杂效应。IgE和抗原之间的平衡可能是调节细胞活化程度的关键。这些结果可能对了解局部持续抗原暴露下过敏性炎症复杂改变的发病机制具有重要意义。

We tested the possibility that IgE crosslinking stimulation may act on FcεRI-bearing cells via paradoxical effects : namely activation versus inhibition of activation. Using human basophils, we found that IgE-mediated weak stimulation consistently induces profound inhibition of basophil releasability against subsequent, IgE-mediated strong stimulation. Intracellular amount of tyrosine kinases, Lyn, Syk, and Btk were semiquantified using intracellular FACS analysis ; however, the amount of these kinases, as shown by their fluorescence intensity, did not change in the treated cells, compared to untreated cells. Interestingly, the delicate balance of IgE and anti-IgE was important in regulating the fate of cellular releasability ; when anti-IgE antibody is too excess, the basophils are immediately activated, but when IgE and anti-IgE antibody are balanced, the cells lose their releasability without releasing their granule contents (demonstrating desensitization).These results imply that IgE-mediated effects on FcεRI-bearing cells are not just cellular stimulation ; IgE can mediate complicated effects on the following IgE-mediated cellular response. The balance between IgE and antigen may be critical in regulating the extent of cellular activation. These results may be important in understanding the pathogenesis of complicated alteration of allergic inflammation under local, continuous antigen exposure.