Coico R F, Berzofsky J A, York-Jolley J, Ozaki S, Siskind G W, Thorbecke G J
J Immunol. 1987 Jan 1;138(1):4-6.
The role of IgD in the immune response has remained elusive, although the predominance of IgD on the B cell surface and the paucity of IgD in serum have suggested a receptor function. In support of this hypothesis, it has recently been shown that receptors for IgD on helper T cells can be induced by exposure to IgD in vivo and in vitro. Such IgD receptor-positive T cells (i.e., T delta cells), detectable as RFC using IgD-coated SRBC, augment antibody responses. In this report, we demonstrate that cloned, antigen-specific T cells of helper phenotype show only very low percentages of IgD-RFC, if allowed to rest in vitro after antigen exposure in the absence of IL 2. Exposure to IgD or to IL 2 for 24 hr causes the IgD-specific RFC to increase as much as 25-fold to nearly 80%. Clones that have recently been stimulated with antigen, or T cell hybridomas prepared from such clones, exhibit 40 to 50% IgD-RFC before exposure and twofold higher levels after exposure to IgD. IL 2 also causes a dose-dependent induction of OgD-RFC in normal splenic T cells. Thus, antigen stimulation, IL 2 and IgD can all induce these receptors for IgD which presumably enable helper T cells to interact more effectively with IgD+ B cells.
尽管B细胞表面IgD占主导地位且血清中IgD含量稀少提示其具有受体功能,但IgD在免疫反应中的作用仍不明确。支持这一假说的是,最近研究表明,在体内和体外接触IgD均可诱导辅助性T细胞上的IgD受体。这种IgD受体阳性T细胞(即Tδ细胞),用IgD包被的SRBC作为RFC可检测到,能增强抗体反应。在本报告中,我们证明,具有辅助表型的克隆化抗原特异性T细胞,若在无IL-2的情况下抗原暴露后于体外静置,其IgD-RFC百分比极低。接触IgD或IL-2 24小时可使IgD特异性RFC增加多达25倍,接近80%。最近用抗原刺激过的克隆,或由此类克隆制备的T细胞杂交瘤,在接触前IgD-RFC为40%至50%,接触IgD后水平升高两倍。IL-2也能在正常脾T细胞中引起剂量依赖性的IgD-RFC诱导。因此,抗原刺激、IL-2和IgD均可诱导这些IgD受体,推测这些受体可使辅助性T细胞更有效地与IgD+B细胞相互作用。