No bones about it: regulatory T cells promote fracture healing
Jason W. Griffith, Andrew D. Luster
Jason W. Griffith, Andrew D. Luster
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No bones about it: regulatory T cells promote fracture healing

Abstract

Regulatory T cells (Tregs) are increasingly being recognized for their role in promoting tissue repair. In this issue of the JCI, Chen et al. found that Tregs at the site of bone injury contribute to bone repair. The CCL1/CCR8 chemokine system promoted the accumulation of Tregs at the site of bone injury, where Tregs supported skeletal stem cell (SSC) accumulation and osteogenic differentiation. CCL1 increased the transcription factor basic leucine zipper ATF-like transcription factor (BATF) in CCR8+ Tregs, which induced the secretion of progranulin that promoted SSC osteogenic function and new bone formation. This study highlights the ever-expanding role of Tregs in tissue repair by demonstrating their ability to expand stem cells at a site of injury.

Authors

Jason W. Griffith, Andrew D. Luster

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Figure 1

Tregs at the site of bone injury contribute to bone repair via the CCL1/CCR8 axis.

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Tregs at the site of bone injury contribute to bone repair via the CCL1/...
Bone fracture induces CCL1 production from bone marrow macrophages, resulting in the accumulation of CCR8+ Tregs at the injury site. CCL1/CCR8 signaling in Tregs induces the expression of the transcription factor BATF, which in turn induces PGRN secretion. PGRN promotes skeletal stem cell differentiation, osteogenic function, and new bone formation.