IL-13 induces proliferation, Ig isotype switching, and Ig synthesis by immature human fetal B cells.
IL-13 induces proliferation, Ig isotype switching, and Ig synthesis by immature human fetal B cells.
复制标题
IL-13 诱导未成熟人胎儿 B 细胞的增殖、Ig 同种型转换和 Ig 合成。
作者：
J. Punnonen;J. D. de Vries
在这项研究中，它表明，新的T细胞衍生的细胞因子IL-13诱导增殖，IG同种型转换，和IG合成的人未成熟B细胞来源于胎儿骨髓（BM）。在抗CD 40单抗或活化的CD 4 + T细胞存在下培养总胎儿BM细胞或高度纯化的s mu+、CD 10+、CD 19+胎儿B细胞时，IL-13诱导增殖和IgM、总IgG、IgG 4和IgE合成。虽然响应IL-13产生的不同同种型的比例与IL-4诱导的相似，但响应IL-13产生的IG水平通常低5- 15倍，表明IL-13的效力低于IL-4。此外，在胎儿B细胞和CD 4 + T细胞克隆的共培养物中，IL-13仅在IL-7存在下有效，这可能是由于与IL-4相反，IL-13不作用于T细胞的事实。IL-6可增强IL-13和IL-4诱导的s mu+、CD 19+胎儿B细胞的IgE合成，IL-12、IFN-α、IFN-γ和转化生长因子-β可抑制IL-13和IL-4诱导的IgE合成，表明IL-13和IL-4通过相似的信号传导途径诱导IgE合成。与IL-4一样，IL-13也通过在活化的克隆CD 4 + T细胞和IL-7存在下共培养的高度纯化的s mu-、CD 10+、CD 19+前B细胞诱导IG产生，包括IgG 4和IgE合成。然而，与IL-4相反，在没有其他刺激的情况下，IL-13不增强培养的s mu-前B细胞上的CD 23、CD 40和HLA-DR表达，这表明单独的IL-13不激活前B细胞。综上所述，我们的数据表明，IL-13诱导增殖，IG同种型转换，和IG生产的未成熟胎儿B细胞的共刺激信号的存在下，由活化的CD 4 + T细胞或抗CD 40单克隆抗体。IL-13是除IL-4之外的另一种细胞因子，其可诱导未成熟人B细胞中同种型转换为IgG 4和IgE合成。
In this study it is demonstrated that the novel T cell-derived cytokine IL-13 induces proliferation, Ig isotype switching, and Ig synthesis by human immature B cells derived from fetal bone marrow (BM). IL-13 induced proliferation and IgM, total IgG, IgG4, and IgE synthesis when total fetal BM cells or highly purified s mu+, CD10+, CD19+ fetal B cells were cultured in the presence of anti-CD40 mAb or activated CD4+ T cells. Although the ratios of the different isotypes produced in response to IL-13 were similar to those induced by IL-4, the levels of Ig produced in response to IL-13 were generally 5- to 15-fold lower, indicating that IL-13 is less potent than IL-4. In addition, in co-cultures of fetal B cells and CD4+ T cell clones IL-13 was effective only in the presence of IL-7, which may be due to the fact that IL-13, in contrast to IL-4, does not act on T cells. IL-13- and IL-4-induced IgE synthesis by s mu+, CD19+ fetal B cells was enhanced by IL-6 and inhibited by IL-12, IFN-alpha, IFN-gamma, and transforming growth factor-beta, suggesting that IL-13 and IL-4 induce IgE synthesis via similar signaling pathways. Like IL-4, IL-13 also induced Ig production, including IgG4 and IgE synthesis, by highly purified s mu-, CD10+, CD19+ pre-B cells co-cultured in the presence of activated cloned CD4+ T cells and IL-7. However, in contrast to IL-4, IL-13 did not enhance CD23, CD40, and HLA-DR expression on cultured s mu- pre-B cells in the absence of other stimuli, suggesting that IL-13 alone does not activate pre-B cells. Taken together, our data indicate that IL-13 induces proliferation, Ig isotype switching, and Ig production by immature fetal B cells in the presence of costimulatory signals provided by activated CD4+ T cells or anti-CD40 mAb. IL-13 is another cytokine that, in addition to IL-4, can induce isotype switching to IgG4 and IgE synthesis in immature human B cells.