Suzuki Jun-Ichiro, Miki Satomi, Ushijima Mitsuyasu, Kodera Yukihiro
Central Research Institute, Wakunaga Pharmaceutical Co., Ltd., Hiroshima 739-1195, Japan.
Exp Ther Med. 2020 Feb;19(2):1570-1573. doi: 10.3892/etm.2019.8392. Epub 2019 Dec 27.
Autophagy is a key event in cellular recycling processes due to its involvement in the intracellular degradation of proteins. It has been demonstrated that -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 and . 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 , and eventually leads to the inhibition of interleukin (IL)-6 production and C-C motif chemokine ligand 2 () mRNA expression . S1PC also increases the level of intestinal immunoglobulin A (IgA) and the number of IgA-producing cells in Peyer's patches . In addition, S1PC triggers the mRNA expression of X-box binding protein 1 (), 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 mRNA expression. The present review summarizes the mechanisms through which the activation of autophagy by S1PC modulates the immune response.
自噬因其参与蛋白质的细胞内降解而成为细胞回收过程中的关键事件。已证实， aged garlic extract中的一种特征性硫化合物-1-丙烯基半胱氨酸（S1PC）可诱导自噬激活。S1PC通过激活自噬降解Toll样受体（TLR）下游的衔接蛋白髓样分化反应蛋白88（MyD88）。MyD88的降解抑制TLR信号通路，包括白细胞介素1受体相关激酶4（IRAK4）和核因子（NF）-κB p65的磷酸化，最终导致白细胞介素（IL）-6产生和C-C基序趋化因子配体2（）mRNA表达的抑制。S1PC还可增加肠道免疫球蛋白A（IgA）水平以及派尔集合淋巴结中产生IgA的细胞数量。此外，S1PC通过细胞外信号调节激酶（ERK）1/2的磷酸化和mRNA表达抑制因子配对盒蛋白5（Pax5）的降解，触发X盒结合蛋白1（）的mRNA表达，X盒结合蛋白1是产生IgA的细胞分化的诱导因子。本综述总结了S1PC激活自噬调节免疫反应的机制。
