Hikida M, Takai T, Ohmori H
Department of Biotechnology, Faculty of Engineering, Okayama University, Japan.
Immunol Lett. 1992 Aug;33(3):301-6. doi: 10.1016/0165-2478(92)90077-2.
We have reported that prostaglandin E2 (PGE2) is a selective stimulator of the antigen-specific IgE response [6]. Because PGE2 is known to elevate intracellular cAMP, we investigated the regulatory role of cAMP in the production of antigen-specific IgE. Anti-TNP IgE response was induced by stimulating TNP-KLH-primed BALB/c spleen cells with the same antigen in vitro. Addition of 10-100 microM dibutyryl cAMP (DBcAMP) to the lymphocyte culture resulted in a 2-3-fold increase in anti-TNP IgE response without affecting the production of anti-TNP IgG1 or IgM. Forskolin, a stimulator of adenylate cyclase, also specifically augmented the IgE response. In contrast, 2',5'-dideoxyadenosine, an inhibitor of adenylate cyclase, suppressed IgE production in an isotype-specific manner. These results suggest that IgE synthesis can be selectively modulated by intracellular cAMP level. Enhancement of IgE production by DBcAMP was observed, particularly in highly primed spleen cells, suggesting that IgE-committed B cells are subjected to regulation by cAMP.
我们曾报道过前列腺素E2（PGE2）是抗原特异性IgE反应的选择性刺激物[6]。由于已知PGE2可提高细胞内cAMP水平，我们研究了cAMP在抗原特异性IgE产生中的调节作用。通过在体外使用相同抗原刺激经TNP-KLH致敏的BALB/c脾细胞来诱导抗TNP IgE反应。向淋巴细胞培养物中添加10 - 100微摩尔的二丁酰cAMP（DBcAMP）可使抗TNP IgE反应增加2至3倍，而不影响抗TNP IgG1或IgM的产生。腺苷酸环化酶刺激剂福斯高林也特异性地增强了IgE反应。相反，腺苷酸环化酶抑制剂2'，5'-二脱氧腺苷以同型特异性方式抑制IgE产生。这些结果表明，IgE合成可被细胞内cAMP水平选择性调节。观察到DBcAMP可增强IgE产生，尤其是在高度致敏的脾细胞中，这表明已定向产生IgE的B细胞受到cAMP的调节。
