Berghmans Nele, Dillen Chris, Heremans Hubertine
Laboratory of Immunobiology, Rega Institute, University of Leuven Medical School, Minderbroedersstraat 10, B-3000 Leuven, Belgium.
J Neuroimmunol. 2006 Jul;176(1-2):63-75. doi: 10.1016/j.jneuroim.2006.04.009. Epub 2006 Jun 9.
Endogenous IL-12 is considered to be required for the generation and function of pathogenic Th1 effector cells in experimental autoimmune encephalomyelitis (EAE). We show here that IL-12 administration together with the immunization suppressed actively induced CREAE in SJL/J and in Biozzi/ABH mice and even subsequent spontaneous relapse incidence and severity in Biozzi ABH mice. IL-12 given during remission of primary disease inhibited re-induced relapses in SJL/J, but not spontaneous relapses in Biozzi mice. The protective effect of IL-12 is time- and dose-dependent. Protection is accompanied by subsequent increased production of IL-10 and IL-5 by lymph node and spleen cells and an inhibition of cell proliferation. Mice depleted of IFN-gamma by administration of neutralizing antibodies were poorly protected by exogenous IL-12, indicating that the inhibitory effect of IL-12 is partially IFN-gamma dependent.
内源性白细胞介素-12（IL-12）被认为是实验性自身免疫性脑脊髓炎（EAE）中致病性Th1效应细胞产生和发挥功能所必需的。我们在此表明，在SJL/J和Biozzi/ABH小鼠中，IL-12与免疫接种一起给药可抑制主动诱导的CREAE，甚至还能降低Biozzi ABH小鼠随后的自发复发发生率和严重程度。在原发性疾病缓解期给予IL-12可抑制SJL/J小鼠再次诱导的复发，但不能抑制Biozzi小鼠的自发复发。IL-12的保护作用具有时间和剂量依赖性。保护作用伴随着随后淋巴结和脾细胞中IL-10和IL-5产生的增加以及细胞增殖的抑制。通过给予中和抗体耗尽干扰素-γ（IFN-γ）的小鼠对外源性IL-12的保护作用较差，这表明IL-12的抑制作用部分依赖于IFN-γ。
