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.

译文

自噬是细胞再生过程中的关键事件,因为它参与了蛋白质的细胞内降解。已经证明,老化的大蒜提取物中的特征性硫化合物S-1-丙烯基半胱氨酸(S1PC)诱导自噬的激活。 S1PC通过在体内和体外激活自噬来降解Toll样受体(TLR)下游的衔接蛋白髓样分化反应蛋白88(MyD88)。 MyD88的降解会抑制TLR信号传导途径,包括体外的白介素1受体相关激酶4(IRAK4)和核因子(NF)-κBp65的磷酸化,最终导致抑制白介素1(IL)-6的产生。体外和CC基序趋化因子配体2(Ccl2)mRNA的体内表达。 S1PC还可以提高体内Peyer斑块中肠道免疫球蛋白A(IgA)的水平和产生IgA的细胞的数量。此外,S1PC触发X-box结合蛋白1(Xbp1)的mRNA表达,X-box结合蛋白1通过细胞外信号调节激酶(ERK)1/2的磷酸化和配对盒蛋白5的降解而诱导产生IgA的细胞分化。 (Pax5),Xbp1 mRNA表达的抑制剂。本综述总结了S1PC激活自噬调节免疫反应的机制。

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