Coffman R L, Shrader B, Carty J, Mosmann T R, Bond M W
DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, CA 94304.
J Immunol. 1987 Dec 1;139(11):3685-90.
Supernatants from a subset of helper T cell clones can enhance IgA, IgE, and IgG1 production in cultures of lipopolysaccharide-stimulated, T cell-depleted spleen cells. The lymphokine interleukin (IL)-4 has been shown to cause the IgE and IgG1 enhancement produced by these supernatants. IgA enhancement, however, is mediated by a factor distinct from IL-4, although IL-4 can potentiate the effect of the IgA-enhancing factor. IgA-enhancing factor is also distinct from IL-1, IL-2, IL-3, granulocyte-macrophage colony-stimulating factor, and interferon-gamma and acts directly on B cells. Purified IgA-enhancing factor enhances IgA production three- to sixfold yet causes less than a twofold increase in other isotypes. The IgA enhancing activity is not inhibited by concentrations of interferon-gamma that inhibit IL-4 activities. In the accompanying article, we show that this IgA enhancing activity is a novel property of the lymphokine IL-5.
一部分辅助性T细胞克隆的上清液能够增强脂多糖刺激的、T细胞耗尽的脾细胞培养物中IgA、IgE和IgG1的产生。淋巴因子白细胞介素（IL）-4已被证明可导致这些上清液产生IgE和IgG1增强作用。然而，IgA增强作用是由一种不同于IL-4的因子介导的，尽管IL-4可增强IgA增强因子的作用。IgA增强因子也不同于IL-1、IL-2、IL-3、粒细胞-巨噬细胞集落刺激因子和干扰素-γ，并且直接作用于B细胞。纯化的IgA增强因子可使IgA产生增加三至六倍，但导致其他同种型增加不到两倍。IgA增强活性不受抑制IL-4活性的干扰素-γ浓度的抑制。在随附的文章中，我们表明这种IgA增强活性是淋巴因子IL-5的一种新特性。
