Abstract:
:Alternatively activated (M2) macrophages promote wound healing but weaken antimicrobial defenses. The mechanisms that enforce macrophage divergence and dictate the phenotypic and metabolic characteristics of M2 macrophages remain elusive. We show that alternative activation with interleukin (IL)-4 induces expression of metallothionein 3 (MT3) that regulates macrophage polarization and function. MT3 was requisite for metabolic reprograming in IL-4-stimulated macrophages or M(IL-4) macrophages to promote mitochondrial respiration and suppress glycolysis. MT3 fostered an M(IL-4) phenotype, suppressed hypoxia inducible factor (HIF)1α activation, and thwarted the emergence of a proinflammatory M1 program in macrophages. MT3 deficiency augmented macrophage plasticity, resulting in enhanced interferon γ (IFNγ) responsiveness and a dampened M(IL-4) phenotype. Thus, MT3 programs the phenotype and metabolic fate of M(IL-4) macrophages.
journal_name
Cell Repjournal_title
Cell reportsauthors
Chowdhury D,Alrefai H,Landero Figueroa JA,Candor K,Porollo A,Fecher R,Divanovic S,Deepe GS Jr,Subramanian Vignesh Kdoi
10.1016/j.celrep.2019.05.093subject
Has Abstractpub_date
2019-06-25 00:00:00pages
3873-3886.e7issue
13issn
2211-1247pii
S2211-1247(19)30732-6journal_volume
27pub_type
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