Regulation of the polymeric immunoglobulin receptor by the classical and alternative NF-κB pathways in intestinal epithelial cells.
Regulation of the polymeric immunoglobulin receptor by the classical and alternative NF-κB pathways in intestinal epithelial cells.
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聚合免疫球蛋白受体（pIgR）通过肠上皮细胞（IECs）转运IgA抗体。通过激活核因子-κB (NF-κB)，促炎信号通路上调pIgR的表达。在这里，我们研究了在肿瘤坏死因子（TNF）、脂多糖（LPS； toll样受体4 （TLR4）配体）和多肌苷：多胱甘酸（pIC； TLR3配体）刺激HT-29人IEC细胞系后，NF-κB依赖rela的经典途径和relb依赖的替代途径对pIgR调控的贡献。促炎基因如白细胞介素-8 （IL-8）的诱导只需要RelA，而pIgR的表达则受到RelA和RelB共同参与的复杂机制的调控。通过连接淋巴毒素β受体来上调pIgR的表达，提示其直接作用于NF-κB通路。抑制丝裂原活化蛋白激酶可降低IL-8的诱导，但可增强TNF和TLR信号对pIgR的诱导。通过独特的信号通路调节pIgR可以使iec维持高水平的IgA运输，同时限制促炎反应。
The polymeric immunoglobulin receptor (pIgR) transports IgA antibodies across intestinal epithelial cells (IECs). Expression of pIgR is upregulated by proinflammatory signaling pathways via activation of nuclear factor-κB (NF-κB). Here, we examined the contributions of the RelA-dependent classical and RelB-dependent alternative pathways of NF-κB to pIgR regulation in the HT-29 human IEC line following stimulation with tumor necrosis factor (TNF), lipopolysaccharide (LPS; Toll-like receptor 4 (TLR4) ligand), and polyinosinic: polycytidylic acid (pIC; TLR3 ligand). Whereas induction of proinflammatory genes such as interleukin-8 (IL-8) required only RelA, pIgR expression was regulated by complex mechanisms that involved both RelA and RelB. Upregulation of pIgR expression by ligation of the lymphotoxin-β receptor suggested a direct role for the alternative NF-κB pathway. Inhibition of mitogen-activated protein kinases reduced the induction of IL-8, but enhanced the induction of pIgR by TNF and TLR signaling. Regulation of pIgR through unique signaling pathways could allow IECs to sustain high levels of IgA transport while limiting the proinflammatory responses.
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