Invariant NKT cells produce IL-17 through IL-23-dependent and -independent pathways with potential modulation of Th17 response in collagen-induced arthritis

Corrigendum in: /ijmm/31/4/998

  • Authors:
    • Y. Yoshiga
    • D. Goto
    • S. Segawa
    • Y. Ohnishi
    • I. Matsumoto
    • S. Ito
    • A. Tsutsumi
    • M. Taniguchi
    • T. Sumida
  • View Affiliations

  • Published online on: September 1, 2008     https://doi.org/10.3892/ijmm_00000032
  • Pages: 369-374
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Abstract

Invariant natural killer T (iNKT) cells play a protective role in the development of certain autoimmune diseases. However, their precise role in the pathogenesis of autoimmune arthritis remains unclear. In this study, we examined the possible contribution of iNKT cells in collagen-induced arthritis (CIA) by using iNKT cell-deficient mice (Jα281−/− mice). CIA in these mice was markedly suppressed and interleukin (IL)-17 production was reduced in a native type II collagen (CII)-specific T cell response. Draining lymph nodes of CII-immunized Jα281−/− mice contained a significantly low number of IL-17-producing T helper cells. To determine whether iNKT cells produce IL-17, we measured IL-17 by enzyme-linked immunosorbent assay in iNKT cells stimulated with the ligand, α-galactosylceramide (α-GalCer). Notably, splenocytes from Jα281−/− mice stimulated in this way were negative for IL-17, whereas those from C57BL/6 mice produced IL-17. Immunostaining for IL-17 in iNKT cells confirmed intracellular staining of the protein. RT-PCR analysis showed that iNKT cells expressed retinoid-related orphan receptor γT and IL-23 receptor. Moreover, cell sorting demonstrated that NK1.1− iNKT cells were the main producers of IL-17 compared with NK1.1+ iNKT cells. IL-17 production by iNKT cells was induced by IL-23-dependent and -independent pathways, since iNKT produced IL-17 when stimulated with either IL-23 or α-GalCer alone. Our findings indicate that iNKT cells are producers and activators of IL-17 via IL-23- dependent and -independent pathways, suggesting that they are key cells in the pathogenesis of CIA through IL-17.

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September 2008
Volume 22 Issue 3

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Yoshiga Y, Goto D, Segawa S, Ohnishi Y, Matsumoto I, Ito S, Tsutsumi A, Taniguchi M and Sumida T: Invariant NKT cells produce IL-17 through IL-23-dependent and -independent pathways with potential modulation of Th17 response in collagen-induced arthritis Corrigendum in /ijmm/31/4/998. Int J Mol Med 22: 369-374, 2008.
APA
Yoshiga, Y., Goto, D., Segawa, S., Ohnishi, Y., Matsumoto, I., Ito, S. ... Sumida, T. (2008). Invariant NKT cells produce IL-17 through IL-23-dependent and -independent pathways with potential modulation of Th17 response in collagen-induced arthritis Corrigendum in /ijmm/31/4/998. International Journal of Molecular Medicine, 22, 369-374. https://doi.org/10.3892/ijmm_00000032
MLA
Yoshiga, Y., Goto, D., Segawa, S., Ohnishi, Y., Matsumoto, I., Ito, S., Tsutsumi, A., Taniguchi, M., Sumida, T."Invariant NKT cells produce IL-17 through IL-23-dependent and -independent pathways with potential modulation of Th17 response in collagen-induced arthritis Corrigendum in /ijmm/31/4/998". International Journal of Molecular Medicine 22.3 (2008): 369-374.
Chicago
Yoshiga, Y., Goto, D., Segawa, S., Ohnishi, Y., Matsumoto, I., Ito, S., Tsutsumi, A., Taniguchi, M., Sumida, T."Invariant NKT cells produce IL-17 through IL-23-dependent and -independent pathways with potential modulation of Th17 response in collagen-induced arthritis Corrigendum in /ijmm/31/4/998". International Journal of Molecular Medicine 22, no. 3 (2008): 369-374. https://doi.org/10.3892/ijmm_00000032