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We thus compared the lymphopenic environment obtained by irradiation (8?Gy) with that induced by thymectomy and antibody-mediated T cell depletion (T+mAb). The degree and kinetics of lymphopenia associated with the two treatments were similar (not shown). Similarly, the pattern of donor T cell distribution (CFSE+CD3+) in CLN, MLN, SP, and BM between irradiated and T-cell depleted recipients did not differ (Fig?4, T+mAb). However, a significantly higher number of donor T cells was observed in all secondary lymphoid organs of irradiated recipients http://www.selleck.cn/products/ON-01910.html compared to T-cell depleted hosts (T+mAb vs. IRR P? http://www.selleckchem.com/products/abc294640.html compartment, suggesting that homeostatic expansion only partly contributes to the effects of irradiation on T cell trafficking. The frequency of host-reactive T cells mediating GVHD is higher in the naive T-cell compartment (Anderson et?al, 2003). Although controversial, some studies have suggested http://www.selleckchem.com/products/loxo-101.html that memory T cells might not induce GVHD due to their inability to home to secondary lymphoid organs and being re-activated (Chen et?al, 2004; Zheng et?al, 2009). However, as memory T cells can be directly re-activated in non-lymphoid tissue (Sallusto et?al, 1999), and they are able to mediate GVL (Zheng et?al, 2008), we analysed the effect of irradiation-induced damage on memory T-cell trafficking to lymphoid and non-lymphoid tissues. H2-Db�Crestricted HY-specific T effector memory (TEM) CD8+ T cells (David et?al, 2009) were injected i.v. into irradiated or non-irradiated syngeneic female (non-antigenic) mice. These T cells expressed high levels of CD44 and PSGL-1 and did not express CD62L, CCR7 and ��4��7 molecules (not shown) and were previously shown not to migrate to lymph nodes or the gut in physiological conditions (Mirenda et?al, 2007). After irradiation, TEM cells were able to localize to CLN, MLN, SP and BM of irradiated but not of non-irradiated mice (P?