Effects of Exogenous Interleukin-10 in a Murine Model of Graft-Versus-Host Disease to Minor Histocompatibility Antigens

Differential effects of the absence of interferon-gamma and IL-4 in acute graft-versus-host disease after allogeneic bone marrow transplantation in mice.

“…It has been reported that TH2 cells and cytokines can both suppress and augment GVHD (9,10,11,26,27). It is clear that the model used to assess effects on GVHD may be key as some strain combinations (i.e., BALB/c into BALB/c ϫ C57BL/6 F1) can result in a GVHD with autoimmune-like sequelae and antibodies to IL-4 have been reported to be protective in this instance (28).…”

Donor-derived interferon gamma is required for inhibition of acute graft-versus-host disease by interleukin 12.

“…However, not all studies support this simple Th1-Th2 paradigm in the pathogenesis of GVHD. For example, treatment with IL-10 led to inhibition of Th1 responses and IFN-␥ production in allogeneic BMT recipients, but had no protective effect against GVHD-associated weight loss and mortality (35). In addition, administration of exogenous IFN-␥ has been shown to markedly inhibit GVHD (21), and results from our own and others studies have shown that neutralizing IFN-␥ with mAb has no significant inhibitory effect on the development of acute GVHD (9,36).…”

Pretreatment of donors with interleukin-18 attenuates acute graft-versus-host disease via STAT6 and preserves graft-versus-leukemia effects

“…21 Furthermore, other studies have failed to demonstrate a reduction in acute GVHD after direct in vivo administration of T H 2 cytokines to the recipients. [21][22][23][24][25][26] IL-18, as well as its inhibitor IL-18-binding protein, is elevated in acute GVHD. [27][28][29][30] We have previously demonstrated that administration of IL-18 to recipient mice early after BMT reduces the severity of acute GVHD in an IFN-␥-dependent fashion.…”