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Int J Hematol. 2011 May;93(5):571-577. doi: 10.1007/s12185-011-0803-1. Epub 2011 Mar 8.

Implications of TNF-α in the pathogenesis and management of GVHD.

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University of Michigan Blood and Marrow Transplantation Program, 5303 Cancer Center, 1500 E. Medical Center Drive, Ann Arbor, MI, 48109-5941, USA.


Clinical graft-versus-host disease (GVHD) symptoms are the result of a complex set of interactions between cellular and soluble factors. One of the key soluble factors is the proinflammatory cytokine, TNF-α, which participates in the initiating events that culminate in GVHD as well as amplifies the disease process once established. The importance of TNF-α in this process has been supported by a series of clinical experiments demonstrating strong correlation between TNF receptor-1 levels and GVHD. TNF-α has both indirect effects, through activating and proliferation pathways of T cells, the main cellular effector of GVHD, and direct effects leading to apoptosis, on GVHD target tissues. Accordingly, TNF-α has been used as a therapeutic target in experimental GVHD prevention and treatment strategies with promising clinical results. TNF-α can be pharmacologically inhibited using soluble TNF receptors or monoclonal antibodies. The optimal dosing and duration of TNF inhibition to prevent or treat GVHD remains under investigation.

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