γδT, but not αβT, cells prone to migrate into MRONJ site in both humans and mice.
Upon activation, γδT cells produce more sSema4D than αβT cells, in vitro.
sSema4D promotes the production of TNF-α from macrophages.
γδT-KO mice neither develop MRONJ nor produce sSema4D or TNF-α in the lesion.
Anti-Sema4D mAb suppressed the onset of MRONJ in wild-type mice.