A Special Population of Regulatory T Cells Potentiates Muscle Repair

被引:917
作者
Burzyn, Dalia [1 ]
Kuswanto, Wilson [1 ]
Kolodin, Dmitriy [1 ]
Shadrach, Jennifer L. [2 ,3 ]
Cerletti, Massimiliano [2 ]
Jang, Young [2 ]
Sefik, Esen [1 ]
Tan, Tze Guan [1 ]
Wagers, Amy J. [2 ,3 ]
Benoist, Christophe [1 ]
Mathis, Diane [1 ]
机构
[1] Harvard Univ, Sch Med, Boston, MA 02115 USA
[2] Harvard Univ, Cambridge, MA 02138 USA
[3] Howard Hughes Med Inst, Chevy Chase, MD 20815 USA
关键词
GROWTH-FACTOR; UNIQUE POPULATION; SYSTEM; DIFFERENTIATION; AMPHIREGULIN; REGENERATION; CYTOKINE; SURVIVAL; SUBSETS; MICE;
D O I
10.1016/j.cell.2013.10.054
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Long recognized to be potent suppressors of immune responses, Foxp3(+)CD4(+) regulatory T (Treg) cells are being rediscovered as regulators of nonimmunological processes. We describe a phenotypically and functionally distinct population of Treg cells that rapidly accumulated in the acutely injured skeletal muscle of mice, just as invading myeloid-lineage cells switched from a proinflammatory to a proregenerative state. A Treg population of similar phenotype accumulated in muscles of genetically dystrophic mice. Punctual depletion of Treg cells during the repair process prolonged the proinflammatory infiltrate and impaired muscle repair, while treatments that increased or decreased Treg activities diminished or enhanced (respectively) muscle damage in a dystrophy model. Muscle Treg cells expressed the growth factor Amphiregulin, which acted directly on muscle satellite cells in vitro and improved muscle repair in vivo. Thus, Treg cells and their products may provide new therapeutic opportunities for wound repair and muscular dystrophies.
引用
收藏
页码:1282 / 1295
页数:14
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