Kim Hyun Jung, Hwang Su Jin, Kim Byoung Kwon, Jung Kyeong Cheon, Chung Doo Hyun
Department of Pathology, Seoul National University College of Medicine, Chongno-gu, Seoul, Korea.
Immunology. 2006 May;118(1):101-11. doi: 10.1111/j.1365-2567.2006.02346.x.
Oral tolerance is the systemic unresponsiveness induced by orally administered proteins. To explore the roles of natural killer T (NKT) cells in oral tolerance, we induced oral tolerance to ovalbumin (OVA) in NKT cell-deficient mice. In CD1d-/- mice, the induction of tolerance to orally administered high- or low-dose OVA was impaired. Dendritic cells (DCs) in the Peyer's patches (PPs) of CD1d-/- mice fed OVA showed high expression of major histocompatibility complex (MHC) class II and B7 molecules, whereas DCs of control mice fed OVA expressed low levels of these molecules. The adoptive transfer of NKT cells restored oral tolerance and induction of tolerogenic DCs in the PPs and spleens of CD1d-/- mice. Moreover, interleukin (IL)-10 and transforming growth factor (TGF)-beta1 production in vitro were reduced in cells from the spleen and PPs of CD1d-/- mice compared with those of control mice fed OVA. The numbers of OVA-specific CD4+ KJ1-26+ T cells were significantly reduced in the PPs and spleens of DO11.10 mice fed OVA. In contrast, OVA-specific CD4+ KJ1-26+ T cells were not deleted in the PPs or spleens of DO11.10 CD1d-/- mice. In conclusion, NKT cells were found to play an indispensable role in oral tolerance by inducing regulatory T cells, and clonally deleting antigen-specific CD4+ T cells.
口服耐受是由口服蛋白质诱导产生的全身性无反应状态。为了探究自然杀伤T(NKT)细胞在口服耐受中的作用,我们在NKT细胞缺陷小鼠中诱导了对卵清蛋白(OVA)的口服耐受。在CD1d基因敲除小鼠中,对口服高剂量或低剂量OVA的耐受诱导受损。给喂食OVA的CD1d基因敲除小鼠的派尔集合淋巴结(PPs)中的树突状细胞(DCs)高表达主要组织相容性复合体(MHC)II类分子和B7分子,而给喂食OVA的对照小鼠的DCs表达这些分子的水平较低。NKT细胞的过继转移恢复了CD1d基因敲除小鼠PPs和脾脏中的口服耐受以及耐受性DCs的诱导。此外,与给喂食OVA的对照小鼠相比,CD1d基因敲除小鼠脾脏和PPs中的细胞在体外产生的白细胞介素(IL)-10和转化生长因子(TGF)-β1减少。给喂食OVA的DO11.10小鼠的PPs和脾脏中OVA特异性CD4⁺ KJ1-26⁺ T细胞数量显著减少。相比之下,在DO11.10 CD1d基因敲除小鼠的PPs或脾脏中,OVA特异性CD4⁺ KJ1-26⁺ T细胞未被清除。总之,发现NKT细胞通过诱导调节性T细胞和克隆清除抗原特异性CD4⁺ T细胞在口服耐受中发挥不可或缺的作用。