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

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Abstract

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.

Original languageEnglish
Pages (from-to)571-577
Number of pages7
JournalInternational Journal of Hematology
Volume93
Issue number5
DOIs
StatePublished - May 2011
Externally publishedYes

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