脂解
CD36
过氧化物酶体
清道夫受体
细胞生物学
氧化磷酸化
化学
生物
生物化学
脂肪组织
受体
胆固醇
脂蛋白
作者
Stanley Ching‐Cheng Huang,Bart Everts,Yulia Ivanova,David O’Sullivan,Márcia Nascimento,Amber M. Smith,Wandy L. Beatty,Latisha Love‐Gregory,Wing Y. Lam,Christina M. O’Neill,Cong Yan,Hong Du,Nada A. Abumrad,Joseph F. Urban,Maxim N. Artyomov,Erika L. Pearce,Edward J. Pearce
摘要
Alternatively activated (M2) macrophages use fatty acid oxidation for their metabolic needs. Pearce and colleagues show that triacylglycerols metabolized by lysosomal acid lipase are required for the M2 activation of and function of macrophages. Alternative (M2) activation of macrophages driven via the α-chain of the receptor for interleukin 4 (IL-4Rα) is important for immunity to parasites, wound healing, the prevention of atherosclerosis and metabolic homeostasis. M2 polarization is dependent on fatty acid oxidation (FAO), but the source of the fatty acids that support this metabolic program has not been clear. We found that the uptake of triacylglycerol substrates via the scavenger receptor CD36 and their subsequent lipolysis by lysosomal acid lipase (LAL) was important for the engagement of elevated oxidative phosphorylation, enhanced spare respiratory capacity (SRC), prolonged survival and expression of genes that together define M2 activation. Inhibition of lipolysis suppressed M2 activation during infection with a parasitic helminth and blocked protective responses to this pathogen. Our findings delineate a critical role for cell-intrinsic lysosomal lipolysis in M2 activation.
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