van Egmond M, van Garderen E, van Spriel A B, Damen C A, van Amersfoort E S, van Zandbergen G, van Hattum J, Kuiper J, van de Winkel J G
Department of Immunology and Medarex Europe, University Medical Center Utrecht, Lundlaan 6, 3584 EA Utrecht, The Netherlands.
Nat Med. 2000 Jun;6(6):680-5. doi: 10.1038/76261.
Despite the well-recognized involvement of immunoglobulin (Ig) A in mucosal immunity, the function of its receptor, FcalphaRI (CD89), is poorly understood. The ability of FcalphaRI to activate leukocytes seems to conflict with the proposed anti-inflammatory activity of secretory IgA. We show here that in a transgenic mouse model, inflammatory mediators induced expression of FcalphaRI on Kupffer cells, which enabled efficient phagocytosis in vivo of bacteria coated with serum IgA. Secretory IgA did not initiate phagocytosis. Therefore, interactions between serum IgA and FcalphaRI on Kupffer cells may provide a 'second line of defense' in mucosal immunity, by eliminating invasive bacteria entering through the portal circulation and thus preventing disease.
尽管免疫球蛋白(Ig)A在黏膜免疫中的作用已得到广泛认可,但其受体FcalphaRI(CD89)的功能却鲜为人知。FcalphaRI激活白细胞的能力似乎与分泌型IgA所具有的抗炎活性相矛盾。我们在此表明,在一个转基因小鼠模型中,炎症介质可诱导库普弗细胞表达FcalphaRI,从而使其能够在体内有效吞噬被血清IgA包被的细菌。分泌型IgA不会启动吞噬作用。因此,血清IgA与库普弗细胞上的FcalphaRI之间的相互作用可能通过清除经门静脉循环进入的入侵细菌并预防疾病,在黏膜免疫中提供“第二道防线”。