Serum cytokine levels and acute graft-versus-host disease after HLA-identical hematopoietic stem cell transplantation

Interleukin-17–Producing T-Helper Cells as New Potential Player Mediating Graft-Versus-Host Disease in Patients Undergoing Allogeneic Stem-Cell Transplantation

“…We hypothesize that the enhancement of the TH-17 population in GVHD patients could be supported by the proinflammatory environment characterizing the active phases of the disease. In fact, in agreement with the results already reported in the literature (23,24), we demonstrated that patients with aGVHD or with active of cGVHD show enhanced plasma levels of several inflammatory mediators (TNF-␣, IL-6, and IL-8). In addition, it has been established that a decrease in TGF-␤ levels after transplant engraftment was significantly associated with aGVHD (24).…”

“…However, it has been demonstrated that this increase has been not significantly related to the severity of aGVHD (40). In accordance with data obtained from other groups (24,41,42), our results did not show an association between the IFN-␥ plasma levels and the activation status of GVHD. In addition, we did not find a correlation between the IFN-␥ levels and the amount of IL-17 ϩ IFN-␥ ϩ CD4 ϩ cells.…”

Functional Myeloid-Derived Suppressor Cell Subsets Recover Rapidly after Allogeneic Hematopoietic Stem/Progenitor Cell Transplantation

“…Serum levels of IFN-g, TNF-a, and IL-6 are increased in the first 2 to 3 weeks after allo-HSCT [28,29], and G-CSF was also increased in patients posttransplantation [10]. Our data show that both MDSC subsets recovered within 1 month post-transplantation.…”

“…Interestingly, these growth factors and proinflammatory cytokines, which can induce the differentiation and activate MDSCs, have also been found to be important in the pathogenesis of GVHD [27,28]. Serum levels of IFN-g, TNF-a, and IL-6 are increased in the first 2 to 3 weeks after allo-HSCT [28,29], and G-CSF was also increased in patients posttransplantation [10].…”

Harnessing the power of alloreactivity without triggering graft-versus-host disease: how non-engrafting alloreactive cellular therapy might change the landscape of acute myeloid leukemia treatment

“…No significant changes were seen for a plethora of other cytokines (including IL-2, IL-4, IL-1β, IL-12, IL-17, IFN-α, granulocytemacrophage colony stimulating factor, and G-CSF). Although detailed patient-level analysis is needed, this preliminary work suggests that the NEACT cytokine profile may differ from early acute GVHD [92][93][94][95][96][97][98] and from engraftment syndrome [94]. Intriguingly, it may share the greatest similarities with "autologous GVHD" [99] and with chimeric antigen receptor-transduced autologous T cell immunotherapy [100,101].…”