Macrophages and monocytes take a portion of the debris left over from the digestion of a pathogen and present it as an antigen to the adaptive immune system. Phagocytosis of apoptotic inflammatory cells is one of mechanisms by which inflammation is eliminated. TLR4 signaling was found to be necessary and sufficient for phagocytosis by monocytes. Phagocytosis was found to be correlated to the immune reaction. The present study indicated that TLR4 overexpression increased the phagocytic capacity of monocytes and macrophages. LPS is recognized by TLR4, which causes the production of NO and the release of inflammatory cytokines, which in turn promote inflammatory cell infiltration. TLR4 up-regulates iNOS transcription. In macrophages, iNOS production is a result of activation by endotoxins and cytokines. The generation of NO help host to kill and inhibit the growth of invading microorganisms and neoplastic tissue. NO directly or indirectly killed or reduced replication of infectious agents, such as viruses, bacteria, protozoa, fungi, helminthes, TNF-a can promote the synthesis of NO. In this transgenic group, NO expressed more NO and peaked 8 hours after LPS challenge. At the same time as NO production, IL-6 and IL-8 transcription increased. This indicated that corresponding to IL-6 and IL-8, NO contributed to inflammatory and anti-inflammatory effects. In summary, Under LPS stimulation, Overexpression TLR4 animals rapidly activated the TLR4 signaling pathway. And this might help host launched the immune response against pathogen invasion and infection. Allogeneic hematopoietic cell transplantation remains a potentially curative treatment for leukemias and lymphomas, but its clinical utility has been limited by morbidity and mortality from graft-vs.-host disease. Thus, the development of strategies to achieve anti-tumor responses without GVHD has been a major goal in the field of allo-HCT. Donor lymphocyte infusion, at doses that would induce lethal GVHD in freshly-irradiated mice, mediates effective anti-tumor responses without severe GVHD in established mixed hematopoietic chimeras. The lack of conditioning-induced inflammation at the time of DLI has been shown to be an important factor that prevents trafficking of alloreactive DLI T cells into the epithelial GVHD target tissues in established MCs. Delayed DLI following the Nutlin-3 establishment of mixed chimerism has also been shown to have the potential to cure hematopoietic malignancies in clinical trials. However, in comparison to mouse studies in which anti-tumor effects can be reliably achieved by delayed DLI without severe GVHD, a higher incidence of GVHD was noted in mixed chimeric patients after DLI. In contrast to patients in whom lymphopenia persisted for many months after conditioning, lymphocytes recovered to normal levels quickly in mice after allo-HCT for the establishment of mixed chimerism. It has been shown that T cell depletion immediately before DLI augments GVHD. It was recently found that established lymphocyte-deficient MCs develop GVHD after DLI, whereas those without lymphopenia do not, indicating that lymphopenia at the time of DLI also promotes GVHD in MCs. In the present study, we assessed the role of donor bone marrow -derived T cells in the development of GVHD in established MCs after DLI. Our data indicate that donor BM-derived T cells, particularly CD8 T cells that develop de novo in MCs are highly protective against GVHD, and that depletion of these T cells.