人U937细胞吞噬IgA免疫复合物的研究

Phagocytosis of IgA immune complexes by human U937 cells

目的 对IgAFc受体 (FcαRⅠ )介导的U937细胞吞噬IgA免疫复合物进行研究。方法以异硫氰酸荧光素 (FITC)标记的 8.9NIP BSA为抗原 ,与抗NIP的IgA或IgG抗体结合 ,分别形成IgA免疫复合物 (IgAIC)和IgG免疫复合物 (IgGIC) ,再与经佛波醇乙酯 (PMA)刺激分化为单核细胞样的U937细胞孵育 ,流式细胞仪分析U937细胞吞噬IgAIC和IgGIC的情况。结果U937细胞表面FcαRⅠ表达量高于 3种IgGFc受体 (FcγRⅠ、FcγRⅡ、FcγRⅢ )。PMA刺激后细胞表面FcαRⅠ上调明显 ,吞噬IgAIC能力增加。FcαRⅠ介导的U937细胞对IgAIC的吞噬作用高于FcγRⅠ和FcγRⅡ介导的对IgGIC的吞噬作用 ,且这种吞噬作用是特异性的。在补体受体CR1和CR3作用下 ,U937细胞对IgAIC的吞噬作用有所增强。结论 FcαRⅠ介导单核细胞非常强的吞噬IgAIC的作用。

Objective Studying FcαRⅠ mediated phagocytosis of IgA immune complexes by U937 cells. Methods Antigen 8.9NIP/BSA was labeled with FITC and then reacted with anti NIP IgA or anti NIP IgG antibodies to form immune complexes (IC). They were then incubated with phorbol 12-myristate 13-acetate (PMA) stimulated U937 cells. The phagocytosed IC was quantified by flow cytometry. Results Expression of FcαRⅠ on U937 cells was higher than that of FcγRⅠ, FcγRⅡ and FcγRⅢ. After stimulation by PMA, expression of FcαRⅠ on U937 cells was markedly upregulated and the phagocytosis of IgA IC was enhanced. FcαRⅠ mediated specific IgA phagocytosis was stronger than FcγRⅠ and FcγRⅡ mediated IgG phagocytosis. Complement receptors, CR1 and CR3, enhanced U937 cell phagocytosis of IgA IC. Conclusion FcαRⅠ mediated strong phagocytosis of IgA IC.