Journal
INTERNATIONAL JOURNAL OF HEMATOLOGY
Volume 93, Issue 5, Pages 571-577Publisher
SPRINGER JAPAN KK
DOI: 10.1007/s12185-011-0803-1
Keywords
Tumor necrosis factor; Graft-versus-host disease; Allogeneic; Bone marrow transplantation; Treatment; Prevention
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Funding
- NCI NIH HHS [P01 CA039542] Funding Source: Medline
- NHLBI NIH HHS [R34 HL105776] Funding Source: Medline
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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-alpha, which participates in the initiating events that culminate in GVHD as well as amplifies the disease process once established. The importance of TNF-alpha in this process has been supported by a series of clinical experiments demonstrating strong correlation between TNF receptor-1 levels and GVHD. TNF-alpha 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-alpha has been used as a therapeutic target in experimental GVHD prevention and treatment strategies with promising clinical results. TNF-alpha 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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