S-Space College of Medicine/School of Medicine (의과대학/대학원) Immunology (면역학전공) Journal Papers (저널논문_면역학전공)
NKT cells play critical roles in the induction of oral tolerance by inducing regulatory T cells producing IL-10 and transforming growth factor beta, and by clonally deleting antigen-specific T cells
- Kim, H. J.; Hwang, S. J.; Kim, B. K.; Jung, K. C.; Chung, D. H.
- Issue Date
- Immunology. 2006 May;118(1):101-11.
- Administration, Oral; Adoptive Transfer; Animals; Clonal Deletion/*immunology; Dendritic Cells/immunology; Dose-Response Relationship, Immunologic; Interleukin-10/*biosynthesis; Killer Cells, Natural/*immunology; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Transgenic; Ovalbumin/immunology; Peyer's Patches/immunology; Spleen/immunology; T-Lymphocytes, Regulatory/*immunology; Transforming Growth Factor beta/*biosynthesis
- 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.
- 0019-2805 (Print)
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