IL17A and bone fracture: As the osteogenic differentiation ability of allo-MSCs was inhibited by IL-17 and IFN-γ (16, 21), the early source of IL-17 in the transplant area was identified as Vγ4T cells (12); thus, we investigated whether HVEM-BTLA signalling could inhibit the function of Vγ4T cells to promote allo-MSC-based TEB repair of bone fractures.