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lüll Pathophysiology of acute graft-versus-host disease: recent advances Sun Y; Tawara I; Toubai T; Reddy PTransl Res 2007[Oct]; 150 (4): 197-214Allogeneic hematopoietic stem cell transplantation (HSCT) is a potentially curative therapy for many malignant and nonmalignant hematologic diseases. Donor T cells from the allografts are critical for the success of this effective therapy. Unfortunately these T cells not only recognize and attack the disease cells/tissues but also the other normal tissues of the recipient as "foreign" or "nonself" and cause severe, immune-mediated toxicity, graft-versus-host disease (GVHD). Several insights into the complex pathophysiology of GVHD have been gained from recent experimental observations, which show that acute GVHD is a consequence of interactions between both the donor and the host innate and adaptive immune systems. These insights have identified a role for a variety of cytokines, chemokines, novel T-cell subsets (naijve, memory, regulatory, and NKT cells) and for non-T cells of both the donor and the host (antigen presenting cells, delta T cells, B cells, and NK cells) in modulating the induction, severity, and maintenance of acute GVHD. This review will focus on the immunobiology of experimental acute GVHD with an emphasis on the recent observations.|Acute Disease[MESH]|Animals[MESH]|Bone Marrow Transplantation/*immunology[MESH]|Chronic Disease[MESH]|Graft vs Host Disease/*immunology/mortality/prevention & control[MESH]|Hematopoietic Stem Cell Transplantation[MESH]|Humans[MESH]|Immunosuppressive Agents/therapeutic use[MESH]|Inflammation Mediators/*immunology[MESH]|Lymphocyte Depletion[MESH]|Minor Histocompatibility Antigens/immunology[MESH]|Myeloablative Agonists/therapeutic use[MESH]|Peripheral Blood Stem Cell Transplantation[MESH]|Risk Factors[MESH]|T-Lymphocytes, Cytotoxic/immunology[MESH]|Transplantation Conditioning[MESH]|Transplantation Immunology/drug effects[MESH]|Transplantation, Homologous/*immunology[MESH] |