Metabolism and acetylation in innate immune cell function and fate.
Innate immunity is the first line of defense against invading pathogens. Changes in both metabolism and chromatin accessibility contribute to the shaping of these innate immune responses, and we are beginning to appreciate that cross-talk between these two systems plays an important role in determining innate immune cell differentiation and function. In this review we focus on acetylation, a post-translational modification important for both regulating chromatin accessibility by modulating histone function, and for functional regulation of non-histone proteins, which has many links to both immune signaling and metabolism. We discuss the interactions between metabolism and acetylation, including the requirement for metabolic intermediates as substrates and co-factors for acetylation, and the regulation of metabolic proteins and enzymes by acetylation. Here we highlight recent findings, which demonstrate the role that the metabolism-acetylation axis has in coordinating the responses of innate immune cells to the availability of nutrients and the microenvironment.
Department of Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, 79108 Freiburg, Germany.
Alanna M
AM
Cameron
Department of Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, 79108 Freiburg, Germany.
Simon J
SJ
Lawless
Department of Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, 79108 Freiburg, Germany; Faculty of Biology, University of Freiburg, 79104 Freiburg, Germany. Electronic address: pearceed@ie-freiburg.mpg.de.
Edward J
EJ
Pearce
D000107:Acetylation; D000818:Animals; D004734:Energy Metabolism; D044127:Epigenesis, Genetic; D005786:Gene Expression Regulation; D006657:Histones / Q000378:metabolism; D006801:Humans; D007107:Immune System / Q000166:cytology* / Q000502:physiology*; D007113:Immunity, Innate; D056747:Immunomodulation; D015398:Signal Transduction
D006657:Histones
Acetylation; Dendritic cells; Immunometabolism; Innate immunity; Macrophages