Chen Y, Inobe J, Weiner H L
Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
J Immunol. 1995 Jul 15;155(2):910-6.
We have previously shown that orally administered myelin basic protein (MBP) suppresses experimental autoimmune encephalomyelitis in both the Lewis rat and the SJL mouse. In the Lewis rat fed low doses of MBP, we found that protection can be adoptively transferred by CD8+ cells and that these cells inhibit immune responses via the secretion of TGF-beta after Ag-specific triggering. In the present study, we investigated the cellular requirements for the generation of active suppression following oral administration of MBP in SJL and (PLJ x SJL)F1 mice. We first determined the frequency of MBP cells secreting Th1 (IFN-gamma) and Th2 (IL-4/IL-10) cytokines or TGF-beta after oral administration of MBP. We found that in SJL mice, orally administered MBP (0.5 mg/feeding) led to an increased frequency of TGF-beta-, IL-4-, and IL-10-secreting cells and a decreased frequency of IFN-gamma-producing cells. This pattern was observed in both CD4+ and CD8+ populations; adoptive transfer of either CD4+ or CD8+ cells from orally tolerized mice suppressed autoimmune encephalomyelitis in recipient animals. We then studied the role of CD8+ cells on the generation of oral tolerance to MBP by depleting CD8+ cells in vivo with anti-CD8 mAb. Oral tolerance was successfully induced in such animals, as demonstrated by a decrease in clinical disease and T cell proliferative responses, although there was less TGF-beta production in vitro and less disease protection on days 20 to 22 in CD8-depleted animals. These studies demonstrate that CD4+ cells in the absence of CD8+ cells can mediate the active suppression component of oral tolerance in mice and that there is a reciprocal relationship between Th1- and Th2-type cytokine production associated with oral tolerization.
我们之前已经表明,口服髓鞘碱性蛋白(MBP)可抑制Lewis大鼠和SJL小鼠的实验性自身免疫性脑脊髓炎。在喂食低剂量MBP的Lewis大鼠中,我们发现保护作用可通过CD8 +细胞进行过继转移,并且这些细胞在抗原特异性触发后通过分泌转化生长因子-β(TGF-β)来抑制免疫反应。在本研究中,我们调查了SJL和(PLJ×SJL)F1小鼠口服MBP后产生主动抑制作用的细胞需求。我们首先确定了口服MBP后分泌Th1(干扰素-γ)和Th2(白细胞介素-4/白细胞介素-10)细胞因子或TGF-β的MBP细胞的频率。我们发现,在SJL小鼠中,口服MBP(每次喂食0.5毫克)导致分泌TGF-β、白细胞介素-4和白细胞介素-10的细胞频率增加,而产生干扰素-γ的细胞频率降低。在CD4 +和CD8 +群体中均观察到这种模式;来自口服耐受小鼠的CD4 +或CD8 +细胞的过继转移均抑制了受体动物的自身免疫性脑脊髓炎。然后,我们通过用抗CD8单克隆抗体在体内清除CD8 +细胞,研究了CD8 +细胞在对MBP产生口服耐受中的作用。在这些动物中成功诱导了口服耐受,临床疾病和T细胞增殖反应均降低,尽管在CD8缺失的动物中,体外TGF-β产生较少,且在第20至22天疾病保护作用较弱。这些研究表明,在没有CD8 +细胞的情况下,CD4 +细胞可介导小鼠口服耐受的主动抑制成分,并且与口服耐受相关的Th1型和Th2型细胞因子产生之间存在相互关系。