Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8633043 | Metabolism | 2018 | 16 Pages |
Abstract
Immunometabolism aims to define the role of intermediary metabolism in immune cell function, with bioenergetics and the mitochondria recently taking center stage. To date, the medical literature on mitochondria and immune function extols the virtues of mouse models in exploring this biologic intersection. While the laboratory mouse has become a standard for studying mammalian biology, this model comprises part of a comprehensive approach. Humans, with their broad array of inherited phenotypes, serve as a starting point for studying immunometabolism; specifically, patients with mitochondrial disease. Using this top-down approach, the mouse as a model organism facilitates further exploration of the consequences of mutations involved in mitochondrial maintenance and function. In this review, we will discuss the emerging phenotype of immune dysfunction in mitochondrial disease as a model for understanding the role of the mitochondria in immune function in available mouse models.
Keywords
TregIOSCAT helper 2 cellsMNGIET helper 1 cellsT helper 17 cellsTh2Th1BMDCNKTRipk3SIRSTh17PRREAENFATMEFCRISPRDAMPsOXPHOSROSdamage associated molecular patternsSTATexperimental autoimmune encephalomyelitisFatty acid oxidationchromatin immunoprecipitationclustered regularly interspaced short palindromic repeatsBioenergeticsSANDOnatural killer T cellT regulatory cellsbone marrow-derived dendritic cellSystemic inflammatory response syndromeFAOPhosphatidylserineOxidative phosphorylationSignal transducer and activator of transcriptionMouse modelsImmunityproline-rich regionmouse embryonic fibroblastMitochondriaKnockdownknockoutPEOProgressive external ophthalmoplegiaCHiPReactive oxygen species
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Authors
Senta M. Kapnick, Susan E. Pacheco, Peter J. McGuire,