Iikura M, Yamaguchi M, Fujisawa T, Miyamasu M, Takaishi T, Morita Y, Iwase T, Moro I, Yamamoto K, Hirai K
Department of Medicine and Physical Therapy, University of Tokyo School of Medicine, Japan.
J Immunol. 1998 Aug 1;161(3):1510-5.
We examined whether secretory IgA (sIgA), known to mediate eosinophil stimulation, has an effect on basophil functions. An immobilized preparation of sIgA, but not of monomeric IgA, induced histamine release (approximately 15% of total histamine contents) from human basophils in vitro. sIgA-induced basophil histamine release was totally dependent on pretreatment with IL-3. IL-5 and granulocyte-macrophage CSF also primed basophils for sIgA-mediated release. Exogenous divalent ions, i.e., Ca2+ and Mg2+, were essential for sIgA-mediated basophil degranulation, and the degranulation was completed within 45 min. A newly synthesized lipid mediator, leukotriene C4, was also liberated from IL-3-primed, sIgA-stimulated basophils. Enzyme digestion experiments revealed that the (Fc)2 x secretory component portion of sIgA is important for sIgA-mediated basophil activation, but the functional binding sites of sIgA on basophils were surmised to be different from FcalphaR. These observations reveal the novel finding that sIgA is able to stimulate basophils as well as eosinophils. Since sIgA is the most abundant Ig isotype in the secretions from mucosal tissues, and basophils are active participants in allergic late-phase reactions, sIgA-mediated basophil mediator release is potentially involved in exacerbation of the inflammation associated with allergic disorders.
我们研究了已知可介导嗜酸性粒细胞刺激的分泌型IgA（sIgA）是否对嗜碱性粒细胞功能有影响。固定化的sIgA制剂而非单体IgA制剂，可在体外诱导人嗜碱性粒细胞释放组胺（约占组胺总量的15%）。sIgA诱导的嗜碱性粒细胞组胺释放完全依赖于白细胞介素-3（IL-3）的预处理。白细胞介素-5（IL-5）和粒细胞-巨噬细胞集落刺激因子（GM-CSF）也可使嗜碱性粒细胞对sIgA介导的释放产生致敏作用。外源性二价离子，即钙离子（Ca2+）和镁离子（Mg2+），对于sIgA介导的嗜碱性粒细胞脱颗粒至关重要，且脱颗粒在45分钟内完成。一种新合成的脂质介质白三烯C4也从经IL-3致敏、sIgA刺激的嗜碱性粒细胞中释放出来。酶消化实验表明，sIgA的（Fc）2×分泌成分部分对于sIgA介导的嗜碱性粒细胞活化很重要，但推测sIgA在嗜碱性粒细胞上的功能结合位点与FcαR不同。这些观察结果揭示了一个新发现，即sIgA能够刺激嗜碱性粒细胞以及嗜酸性粒细胞。由于sIgA是黏膜组织分泌物中最丰富的Ig同种型，且嗜碱性粒细胞是过敏性迟发相反应的活跃参与者，sIgA介导的嗜碱性粒细胞介质释放可能参与了与过敏性疾病相关的炎症加剧过程。
