Regulatory effects of prostaglandin E2 on the growth and differentiation of human B lymphocytes activated through their CD40 antigen.
Regulatory effects of prostaglandin E2 on the growth and differentiation of human B lymphocytes activated through their CD40 antigen.
复制标题
DOI：
10.4049/jimmunol.152.9.4282
复制
发表时间：
1994-05
影响因子：
4.4
通讯作者：
P. Garrone;L. Galibert;F. Rousset;S. Fu;J. Banchereau
中科院分区：
文献类型：
--
作者：
P. Garrone;L. Galibert;F. Rousset;S. Fu;J. Banchereau
本文研究了前列腺素E_2（PGE_2）对人扁桃体B淋巴细胞在有或无IL-4或IL-10的CD_（40）系统中生长和分化的影响。PGE 2（10（-9）至10（-6）M）增强通过其CD 40 Ag激活的B细胞的增殖，但不增强其IG分泌。通过[3 H]TdR摄取和细胞计数测定，PGE 2进一步增强IL-4和IL-10诱导的B细胞生长。IL-10诱导的IgM、IgG和伊加分泌在加入PGE 2后增强2倍至4倍，而IL-4诱导的IgG和IgE分泌被抑制。IgE的产生是特别敏感的，因为对于10（-7）M PGE 2获得约90%的抑制。此外，PGE 2抑制了在CD 40系统中培养的幼稚表面IgD+ B细胞的IgE产生，表明PGE 2可能与IgE转换相关的机制相互作用。PGE 2对由可溶性抗CD 40抗体激活的B细胞的苦参碱诱导的增殖和IG分泌表现出相似的作用。最后，增加cAMP的试剂模拟了PGE 2的作用，表明PGE 2的活性可能取决于cAMP途径的激活。总之，目前的数据表明，PGE 2刺激人CD 40活化的B细胞生长，但不同地调节精氨酸诱导的分化。因此，在支持免疫应答发展的微环境中，感受态细胞如巨噬细胞分泌PGE 2可能参与体液应答的调节。
We have studied the effects of prostaglandin E2 (PGE2) on the growth and differentiation of human tonsillar B lymphocytes cultured in the CD40 system with or without IL-4 or IL-10. PGE2 (10(-9) to 10(-6) M) enhanced proliferation of B cells activated through their CD40 Ag, but not their Ig secretion. PGE2 further potentiated both IL-4- and IL-10-induced B cell growth as determined by [3H]TdR uptake and cellular enumeration. The IL-10-induced IgM, IgG, and IgA secretion was enhanced twofold to fourfold after addition of PGE2, whereas IL-4-induced IgG and IgE secretion was inhibited. The IgE production was particularly sensitive as an approximately 90% inhibition was obtained for 10(-7) M PGE2. In addition, PGE2 inhibited IgE production by naive surface IgD+ B cells cultured in the CD40 system, suggesting that PGE2 may interact with mechanisms involved in IgE switching. PGE2 displayed similar effects on cytokine-induced proliferation and Ig secretion of B cells activated by anti-CD40 Abs used in a soluble form. Finally, the PGE2 effects were mimicked by agents increasing cAMP, indicating that the PGE2 activities are likely to depend on the activation of the cAMP pathway. Altogether, the present data indicate that PGE2 stimulates human CD40-activated B cell growth, but differently modulates cytokine-induced differentiation. Thus, in microenvironments supporting the development of an immune response, the secretion of PGE2 by competent cells such as macrophages may participate in the regulation of the humoral response.