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2015 ; 29
(6
): 2315-26
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Essential role of mitochondrial energy metabolism in Foxp3? T-regulatory cell
function and allograft survival
#MMPMID25681462
Beier UH
; Angelin A
; Akimova T
; Wang L
; Liu Y
; Xiao H
; Koike MA
; Hancock SA
; Bhatti TR
; Han R
; Jiao J
; Veasey SC
; Sims CA
; Baur JA
; Wallace DC
; Hancock WW
FASEB J
2015[Jun]; 29
(6
): 2315-26
PMID25681462
show ga
Conventional T (Tcon) cells and Foxp3(+) T-regulatory (Treg) cells are thought to
have differing metabolic requirements, but little is known of mitochondrial
functions within these cell populations in vivo. In murine studies, we found that
activation of both Tcon and Treg cells led to myocyte enhancer factor 2
(Mef2)-induced expression of genes important to oxidative phosphorylation
(OXPHOS). Inhibition of OXPHOS impaired both Tcon and Treg cell function compared
to wild-type cells but disproportionally affected Treg cells. Deletion of Pgc1?
or Sirt3, which are key regulators of OXPHOS, abrogated Treg-dependent
suppressive function and impaired allograft survival. Mef2 is inhibited by
histone/protein deacetylase-9 (Hdac9), and Hdac9 deletion increased Treg
suppressive function. Hdac9(-/-) Treg showed increased expression of Pgc1? and
Sirt3, and improved mitochondrial respiration, compared to wild-type Treg cells.
Our data show that key OXPHOS regulators are required for optimal Treg function
and Treg-dependent allograft acceptance. These findings provide a novel approach
to increase Treg function and give insights into the fundamental mechanisms by
which mitochondrial energy metabolism regulates immune cell functions in vivo.
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