Abstract
prosurvival properties [5]. Under these condi‐ tions, it is fair to conceive that all activated lymphomyeloid cells expressing the IL‐15R and exposed to GIFT15 would lose their capacity to trigger immune responses. In light of these results, we tested whether the expression of the fusokine could protect xenografted cells from rejection in immune competent animals. While mice lacking GIFT15 rejected all grafted cells, animals treated with the fusokine have toler‐ ated the xenograft [4]. These results suggest that GIFT15 can act as a suppressor agent of allograft rejection and allows for xenotransplant as well and may present an interesting tool for the treat‐ ment of autoimmune diseases. While studying the pharmacological properties of GIFT15 on unfractionated splenocytes in vitro, we observed that the fusokine had a remarkable and unprece‐ dented effect on naive B cells, converting them into suppressor cells of B‐cell ontogeny (h ereafter GIFT15 Bregs) [6].
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