Toll-like Receptor 4 Is a Sensor for Autophagy Associated with Innate Immunity Export

@article{citeulike:3137995, abstract = {Autophagy has recently been shown to be an important component of the innate immune response. The signaling pathways leading to activation of autophagy in innate immunity are not known. Here we showed that Toll-like receptor 4 (TLR4) served as a previously unrecognized environmental sensor for autophagy. Autophagy was induced by lipopolysaccharide (LPS) in primary human macrophages and in the murine macrophage RAW264.7 cell line. We defined a new molecular pathway in which LPS-induced autophagy was regulated through a Toll-interleukin-1 receptor domain-containing adaptor-inducing interferon-β (TRIF)-dependent, myeloid differentiation factor 88 (MyD88)-independent TLR4 signaling pathway. Receptor-interacting protein (RIP1) and p38 mitogen-activated protein kinase were downstream components of this pathway. This signaling pathway did not affect cell viability, indicating that it is distinct from the autophagic death signaling pathway. We further showed that LPS-induced autophagy could enhance mycobacterial colocalization with the autophagosomes. This study links two ancient processes, autophagy and innate immunity, together through a shared signaling pathway.}, author = {Xu, Yi and Jagannath, Chinnaswamy and Liu, Xian-De and Sharafkhaneh, Amir and Kolodziejska, Katarzyna E. and Eissa, Tony N.}, citeulike-article-id = {3137995}, citeulike-linkout-0 = {http://www.immunity.com/content/article/abstract?uid=PIIS1074761307003366}, day = {27}, journal = {Immunity}, keywords = {autophagy, innate\_immunity, tlr4}, month = {July}, number = {1}, pages = {135--144}, posted-at = {2008-08-19 21:22:48}, priority = {0}, title = {Toll-like Receptor 4 Is a Sensor for Autophagy Associated with Innate Immunity}, url = {http://www.immunity.com/content/article/abstract?uid=PIIS1074761307003366}, volume = {27}, year = {2007} }

TY - JOUR ID - citeulike:3137995 L3 - citeulike-article-id:3137995 N2 - Autophagy has recently been shown to be an important component of the innate immune response. The signaling pathways leading to activation of autophagy in innate immunity are not known. Here we showed that Toll-like receptor 4 (TLR4) served as a previously unrecognized environmental sensor for autophagy. Autophagy was induced by lipopolysaccharide (LPS) in primary human macrophages and in the murine macrophage RAW264.7 cell line. We defined a new molecular pathway in which LPS-induced autophagy was regulated through a Toll-interleukin-1 receptor domain-containing adaptor-inducing interferon-β (TRIF)-dependent, myeloid differentiation factor 88 (MyD88)-independent TLR4 signaling pathway. Receptor-interacting protein (RIP1) and p38 mitogen-activated protein kinase were downstream components of this pathway. This signaling pathway did not affect cell viability, indicating that it is distinct from the autophagic death signaling pathway. We further showed that LPS-induced autophagy could enhance mycobacterial colocalization with the autophagosomes. This study links two ancient processes, autophagy and innate immunity, together through a shared signaling pathway. IS - 1 JF - Immunity EP - 144 TI - Toll-like Receptor 4 Is a Sensor for Autophagy Associated with Innate Immunity VL - 27 SP - 135 KW - autophagy KW - innate_immunity KW - tlr4 AU - Xu, Yi AU - Jagannath, Chinnaswamy AU - Liu, Xian-De AU - Sharafkhaneh, Amir AU - Kolodziejska, Katarzyna AU - Eissa, Tony PY - 2007/07/27/ UR - http://www.immunity.com/content/article/abstract?uid=PIIS1074761307003366 ER -