Livingston P G, Toomey S, Kurane I, Janus J, Ennis F A
Department of Medicine, University of Massachusetts Medical Center, Worcester 01655, USA.
Immunol Invest. 1995 May;24(4):619-29. doi: 10.3109/08820139509066862.
Lymphokines play an important role in immune responses to viruses by modulating functions of T lymphocytes. In the present study, we examined the effects of interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-7 (IL-7), and interferon gamma (IFN gamma) on proliferation, cytotoxic activity and lymphokine production of a dengue virus-specific CD8+ human cytotoxic T lymphocyte (CTL) clone. IL-2 and IL-7 induced proliferation of the CD8+ CTL clone in the presence or absence of specific antigen, while IFN gamma suppressed proliferation of the clone. IL-7 and IFN gamma augmented dengue virus-specific cytotoxic activity without inducing non-specific cytotoxic activity, and IL-2 induced non-specific cytotoxic activity. IL-2 induced IFN gamma production by the CD8+ CTL clone. IL-4 and IL-6 did not modulate the functions of the CD8+ CTL clone in these experimental conditions. These results suggest that functions of dengue virus-specific CD8+ CTL are modulated by IL-2, IL-7 and IFN gamma, and that IL-7 is a lymphokine useful to induce growth and to maintain specific cytotoxic activity of CD8+ CTL clones in vitro.
淋巴因子通过调节T淋巴细胞的功能在针对病毒的免疫反应中发挥重要作用。在本研究中,我们检测了白细胞介素-2(IL-2)、白细胞介素-4(IL-4)、白细胞介素-6(IL-6)、白细胞介素-7(IL-7)和干扰素γ(IFNγ)对登革病毒特异性CD8 + 人细胞毒性T淋巴细胞(CTL)克隆的增殖、细胞毒性活性及淋巴因子产生的影响。在存在或不存在特异性抗原的情况下,IL-2和IL-7均可诱导CD8 + CTL克隆增殖,而IFNγ则抑制该克隆的增殖。IL-7和IFNγ可增强登革病毒特异性细胞毒性活性,且不诱导非特异性细胞毒性活性,而IL-2可诱导非特异性细胞毒性活性。IL-2可诱导CD8 + CTL克隆产生IFNγ。在这些实验条件下,IL-4和IL-6未调节CD8 + CTL克隆的功能。这些结果表明,登革病毒特异性CD8 + CTL的功能受IL-2、IL-7和IFNγ调节,且IL-7是一种有助于在体外诱导CD8 + CTL克隆生长并维持其特异性细胞毒性活性的淋巴因子。