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Regulation of immune response by S‑1‑propenylcysteine through autophagy‑mediated protein degradation (Review)

  • Authors:
    • Jun‑Ichiro Suzuki
    • Satomi Miki
    • Mitsuyasu Ushijima
    • Yukihiro Kodera
  • View Affiliations / Copyright

    Affiliations: Central Research Institute, Wakunaga Pharmaceutical Co., Ltd., Hiroshima 739‑1195, Japan
    Copyright: © Suzuki et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1570-1573
    |
    Published online on: December 27, 2019
       https://doi.org/10.3892/etm.2019.8392
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Abstract

Autophagy is a key event in cellular recycling processes due to its involvement in the intracellular degradation of proteins. It has been demonstrated that S‑1‑propenylcysteine (S1PC), a characteristic sulfur compound in aged garlic extract, induces the activation of autophagy. S1PC degrades the adaptor protein myeloid differentiation response protein 88 (MyD88) of downstream of Toll‑like receptor (TLR) by activating autophagy in vitro and in vivo. The degradation of MyD88 inhibits the TLR signaling pathway, including the phosphorylation of interleukin 1 receptor associated kinase 4 (IRAK4) and nuclear factor (NF)‑κB p65 in vitro, and eventually leads to the inhibition of interleukin (IL)‑6 production in vitro and C‑C motif chemokine ligand 2 (Ccl2) mRNA expression in vivo. S1PC also increases the level of intestinal immunoglobulin A (IgA) and the number of IgA‑producing cells in Peyer's patches in vivo. In addition, S1PC triggers the mRNA expression of X‑box binding protein 1 (Xbp1), an inducer of IgA‑producing cell differentiation via the phosphorylation of extracellular signal‑regulated kinase (ERK)1/2 and the degradation of paired box protein 5 (Pax5), a suppressor of Xbp1 mRNA expression. The present review summarizes the mechanisms through which the activation of autophagy by S1PC modulates the immune response.
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Copy and paste a formatted citation
Spandidos Publications style
Suzuki JI, Miki S, Ushijima M and Kodera Y: Regulation of immune response by S‑1‑propenylcysteine through autophagy‑mediated protein degradation (Review). Exp Ther Med 19: 1570-1573, 2020.
APA
Suzuki, J., Miki, S., Ushijima, M., & Kodera, Y. (2020). Regulation of immune response by S‑1‑propenylcysteine through autophagy‑mediated protein degradation (Review). Experimental and Therapeutic Medicine, 19, 1570-1573. https://doi.org/10.3892/etm.2019.8392
MLA
Suzuki, J., Miki, S., Ushijima, M., Kodera, Y."Regulation of immune response by S‑1‑propenylcysteine through autophagy‑mediated protein degradation (Review)". Experimental and Therapeutic Medicine 19.2 (2020): 1570-1573.
Chicago
Suzuki, J., Miki, S., Ushijima, M., Kodera, Y."Regulation of immune response by S‑1‑propenylcysteine through autophagy‑mediated protein degradation (Review)". Experimental and Therapeutic Medicine 19, no. 2 (2020): 1570-1573. https://doi.org/10.3892/etm.2019.8392
Copy and paste a formatted citation
x
Spandidos Publications style
Suzuki JI, Miki S, Ushijima M and Kodera Y: Regulation of immune response by S‑1‑propenylcysteine through autophagy‑mediated protein degradation (Review). Exp Ther Med 19: 1570-1573, 2020.
APA
Suzuki, J., Miki, S., Ushijima, M., & Kodera, Y. (2020). Regulation of immune response by S‑1‑propenylcysteine through autophagy‑mediated protein degradation (Review). Experimental and Therapeutic Medicine, 19, 1570-1573. https://doi.org/10.3892/etm.2019.8392
MLA
Suzuki, J., Miki, S., Ushijima, M., Kodera, Y."Regulation of immune response by S‑1‑propenylcysteine through autophagy‑mediated protein degradation (Review)". Experimental and Therapeutic Medicine 19.2 (2020): 1570-1573.
Chicago
Suzuki, J., Miki, S., Ushijima, M., Kodera, Y."Regulation of immune response by S‑1‑propenylcysteine through autophagy‑mediated protein degradation (Review)". Experimental and Therapeutic Medicine 19, no. 2 (2020): 1570-1573. https://doi.org/10.3892/etm.2019.8392
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