Abstract
Immune cell activation and differentiation occurs concurrently with metabolic reprogramming. This ensures that activated cells generate the energy and substrates necessary to perform their specified function. Likewise, the metabolic programs among different cells of the immune system vary. By targeting different metabolic pathways, these differences allow for selective regulation of immune responses. Further, the relative susceptibility of cells to a metabolic inhibitor is dictated by their metabolic demands; cellular selectivity is based on demand. Therefore, where differences exist in metabolic pathways between healthy and pathogenic cells, there is opportunity for selective regulation with agents lacking intrinsic specificity. There are now a host of studies demonstrating how inhibitors of metabolism (e.g., glycolysis, glutamine metabolism, and fatty acid oxidation) can regulate immune responses and treat immune-mediated pathogenesis. In this brief review we detail how inhibitors of metabolism can be employed to regulate immune responses in both autoimmunity and transplantation.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 999-1005 |
| Number of pages | 7 |
| Journal | Journal of Immunology |
| Volume | 198 |
| Issue number | 3 |
| DOIs | |
| State | Published - Feb 1 2017 |
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ASJC Scopus subject areas
- Immunology
Cite this
Targeting metabolism as a novel therapeutic approach to autoimmunity, inflammation, and transplantation. / Bettencourt, Ian A.; Powell, Jonathan D.
In: Journal of Immunology, Vol. 198, No. 3, 01.02.2017, p. 999-1005.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Targeting metabolism as a novel therapeutic approach to autoimmunity, inflammation, and transplantation
AU - Bettencourt,Ian A.
AU - Powell,Jonathan D.
PY - 2017/2/1
Y1 - 2017/2/1
N2 - Immune cell activation and differentiation occurs concurrently with metabolic reprogramming. This ensures that activated cells generate the energy and substrates necessary to perform their specified function. Likewise, the metabolic programs among different cells of the immune system vary. By targeting different metabolic pathways, these differences allow for selective regulation of immune responses. Further, the relative susceptibility of cells to a metabolic inhibitor is dictated by their metabolic demands; cellular selectivity is based on demand. Therefore, where differences exist in metabolic pathways between healthy and pathogenic cells, there is opportunity for selective regulation with agents lacking intrinsic specificity. There are now a host of studies demonstrating how inhibitors of metabolism (e.g., glycolysis, glutamine metabolism, and fatty acid oxidation) can regulate immune responses and treat immune-mediated pathogenesis. In this brief review we detail how inhibitors of metabolism can be employed to regulate immune responses in both autoimmunity and transplantation.
AB - Immune cell activation and differentiation occurs concurrently with metabolic reprogramming. This ensures that activated cells generate the energy and substrates necessary to perform their specified function. Likewise, the metabolic programs among different cells of the immune system vary. By targeting different metabolic pathways, these differences allow for selective regulation of immune responses. Further, the relative susceptibility of cells to a metabolic inhibitor is dictated by their metabolic demands; cellular selectivity is based on demand. Therefore, where differences exist in metabolic pathways between healthy and pathogenic cells, there is opportunity for selective regulation with agents lacking intrinsic specificity. There are now a host of studies demonstrating how inhibitors of metabolism (e.g., glycolysis, glutamine metabolism, and fatty acid oxidation) can regulate immune responses and treat immune-mediated pathogenesis. In this brief review we detail how inhibitors of metabolism can be employed to regulate immune responses in both autoimmunity and transplantation.
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UR - http://www.scopus.com/inward/citedby.url?scp=85014605811&partnerID=8YFLogxK
U2 - 10.4049/jimmunol.1601318
DO - 10.4049/jimmunol.1601318
M3 - Review article
VL - 198
SP - 999
EP - 1005
JO - Journal of Immunology
T2 - Journal of Immunology
JF - Journal of Immunology
SN - 0022-1767
IS - 3
ER -