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GVHD-free survival using the Cox model stratified on TBI had a HR of 0��8, 96% CI: 0��71�C0��91, P? http://www.selleckchem.com/products/ch5424802.html interaction test for G-CSF-induced GVHD showed that type of conditioning was not important for induction of GVHD. Taken together, this clinical study and the single-centre study suggest that conditioning with http://www.selleckchem.com/products/VX-770.html TBI does not play a major role in G-CSF-induced GVHD. This contrasts with experimental data in mice, where TBI was found to be a prerequisite for GVHD (Morris et?al, 2009). In the mouse model, it was demonstrated that G-CSF could induce natural killer T-cell-dependent alloreactivity and exacerbate GVHD after bone marrow transplantation. It was also found that TBI increased the expression of G-CSF receptors on host dendritic cells, which stimulated a cascade of events leading to exacerbation of acute GVHD. In addition, G-CSF increases the levels of interleukin 2 (IL-2) receptor-�� (Kobayashi et?al, 1999; Remberger & Sundberg, 2005). This may trigger acute GVHD, because expression of IL-2 receptors is elevated during acute GVHD (Remberger & Ringden, 1995; Miyamoto et?al, 1996; Mathias et?al, 2000). Thus, the use or lack of use of TBI cannot http://www.selleck.cn/products/Verteporfin(Visudyne).html explain the different findings regarding an association between G-CSF and GVHD in different clinical studies (Ringden et?al, 2004; Khoury et?al, 2006). Non-relapse mortality was higher in the G-CSF group in the present study, which is in accordance with some studies (Eapen et?al, 2004; Ringden et?al, 2004), but contrasts with the results of some other large studies (Ho et?al, 2003; Khoury et?al, 2006). In the present analysis, NRM was increased in the growth factor group, regardless of whether conditioning involved TBI or chemotherapy alone (Tables?4 and 5). One reason for the increased NRM with the use of growth factors may be the lower risk of GVHD-free survival. Acute and chronic GVHD are major causes of mortality after HSCT (Ringden & Deeg, 1996). It cannot be excluded that G-CSF may increase the risk of opportunistic infections, because G-CSF has been found to be associated with impaired production of IL-12 by Th2-inducing dendritic cells and lack of expression of IL-12 receptor by the IL-4 and the IL-10-producing CD34+ cells (Volpi et?al, 2001). In vitro studies have also shown that G-CSF reduces the production of interferon-�� and IL-4 (Sloand et?al, 2000).