“…The pathophysiology of GVHD involves activated donor T cells that function as alloreactive effector cells and activate other cells, such as B cells and macrophages, leading to an inflammatory cascade that damages host tissue [ 18 ]. In order to counter the effects of activated and alloreactive T cells, PTCy demonstrated the ability to either reduce or impair the function of alloreactive T cells of donor origin, while sparing precursors to stem cell memory T cells, allowing immune reconstitution and engraftment following aHSCT [ 19 , 20 ]. It is also believed that myeloid-derived suppressor cells (MDSCs), a form of immature myeloid cells that do not complete differentiation, are stimulated following exposure to cyclophosphamide and along with suppressing the immune system, MDSCs, in turn, stimulate regulatory T cells (Treg), which provides protection from GVHD [ 21 , 22 , 23 ].…”