Kern D E, Peace D J, Klarnet J P, Cheever M A, Greenberg P D
Department of Microbiology/Immunology, University of Washington, Seattle 98195.
J Immunol. 1988 Oct 15;141(8):2824-30.
The relative contributions of IL-2 and IL-4 during the immune response to the retrovirus-induced tumor, FBL, were examined. Both proliferative and cytolytic responses to FBL were measured and compared to similar responses to minor histocompatibility Ag. The addition of alpha IL-2 partially inhibited FBL-stimulated proliferation of purified L3T4+ T cells and nearly completely inhibited the response of Lyt-2+ T cells, whereas alpha IL-4 partially inhibited the proliferative response of the L3T4+ subset but had no effect on the response of the Lyt-2+ subset. The addition of exogenous IL-4 augmented the proliferative response of both subsets. Therefore, IL-4 is an endogenous growth factor for FBL-induced specific proliferation of the L3T4+ and not the Lyt-2+ population, but both subpopulations can respond to IL-4. Similar examination of anti-FBL CTL responses revealed that alpha IL-2, but not alpha IL-4, inhibited FBL-specific Lyt-2+ CTL generation. However, exogenous IL-4 partially replaced the L3T4+ Th cell activity necessary for optimal Lyt-2+ FBL-specific CTL generation. Therefore, IL-4 is not required but can participate in the CTL response. The role of IL-4 during the immune response of B6 mice to minor histocompatibility Ag disparate BALB.B cells was analyzed. alpha IL-4 had no detectable effect on the proliferative or cytolytic response to BALB.B cells, suggesting that endogenous IL-4 does not have a significant role in these responses. The extent of involvement of endogenous IL-4 in the T cell responses to retrovirus-induced tumor Ag and minor histocompatibility Ag presumably reflects the nature of the stimulating Ag, and detection of an IL-4 response may correlate with induction of an antibody response. Thus, the immunizing Ag and/or host B cell repetoire may influence which subsets of L3T4+ Th cells are activated during priming in vivo.
研究了白细胞介素-2(IL-2)和白细胞介素-4(IL-4)在对逆转录病毒诱导的肿瘤FBL的免疫反应中的相对贡献。测量了对FBL的增殖反应和细胞溶解反应,并与对次要组织相容性抗原的类似反应进行比较。添加αIL-2部分抑制了FBL刺激的纯化L3T4 + T细胞的增殖,并几乎完全抑制了Lyt-2 + T细胞的反应,而αIL-4部分抑制了L3T4 +亚群的增殖反应,但对Lyt-2 +亚群的反应没有影响。添加外源性IL-4增强了两个亚群的增殖反应。因此,IL-4是FBL诱导的L3T4 +而非Lyt-2 +群体特异性增殖的内源性生长因子,但两个亚群均可对IL-4作出反应。对抗FBL细胞毒性T淋巴细胞(CTL)反应的类似研究表明,αIL-2而非αIL-4抑制FBL特异性Lyt-2 + CTL的产生。然而,外源性IL-4部分替代了最佳Lyt-2 + FBL特异性CTL产生所需的L3T4 +辅助性T细胞(Th细胞)活性。因此,IL-4并非必需,但可参与CTL反应。分析了IL-4在B6小鼠对次要组织相容性抗原不同的BALB.B细胞的免疫反应中的作用。αIL-4对BALB.B细胞的增殖或细胞溶解反应没有可检测到的影响,这表明内源性IL-4在这些反应中没有显著作用。内源性IL-4参与对逆转录病毒诱导的肿瘤抗原和次要组织相容性抗原的T细胞反应的程度大概反映了刺激抗原的性质,并且IL-4反应的检测可能与抗体反应的诱导相关。因此,免疫抗原和/或宿主B细胞库可能影响体内启动过程中哪些L3T4 + Th细胞亚群被激活。