Harris James, De Haro Sergio A, Master Sharon S, Keane Joseph, Roberts Esteban A, Delgado Monica, Deretic Vojo
Department of Molecular Genetics and Microbiology, University of New Mexico Health Sciences Center, University of New Mexico School of Medicine, 915 Camino de Salud NE, Albuquerque, NM 87131, USA.
Immunity. 2007 Sep;27(3):505-17. doi: 10.1016/j.immuni.2007.07.022.
Autophagy is a recently recognized immune effector mechanism against intracellular pathogens. The role of autophagy in innate immunity has been well established, but the extent of its regulation by the adaptive immune response is less well understood. The T helper 1 (Th1) cell cytokine IFN-gamma induces autophagy in macrophages to eliminate Mycobacterium tuberculosis. Here, we report that Th2 cytokines affect autophagy in macrophages and their ability to control intracellular M. tuberculosis. IL-4 and IL-13 abrogated autophagy and autophagy-mediated killing of intracellular mycobacteria in murine and human macrophages. Inhibition of starvation-induced autophagy by IL-4 and IL-13 was dependent on Akt signaling, whereas the inhibition of IFN-gamma-induced autophagy was Akt independent and signal transducer and activator of transcription 6 (STAT6) dependent. These findings establish a mechanism through which Th1-Th2 polarization differentially affects the immune control of intracellular pathogens.
自噬是一种最近被认识到的针对细胞内病原体的免疫效应机制。自噬在固有免疫中的作用已得到充分证实,但其受适应性免疫应答调节的程度尚不太清楚。辅助性T细胞1(Th1)细胞因子γ干扰素可诱导巨噬细胞发生自噬,以清除结核分枝杆菌。在此,我们报告Th2细胞因子会影响巨噬细胞中的自噬及其控制细胞内结核分枝杆菌的能力。白细胞介素-4(IL-4)和白细胞介素-13(IL-13)可消除小鼠和人类巨噬细胞中的自噬以及自噬介导的对细胞内分枝杆菌的杀伤作用。IL-4和IL-13对饥饿诱导的自噬的抑制作用依赖于Akt信号传导,而对γ干扰素诱导的自噬的抑制作用不依赖Akt,而是依赖信号转导及转录激活因子6(STAT6)。这些发现确立了一种机制,通过该机制Th1-Th2极化会以不同方式影响对细胞内病原体的免疫控制。