Important note: Information in this article was accurate in 2000. The state of the art may have changed since the publication date.
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Microsc Res Tech. 2000 Aug 1;50(3):229-35. Unique Identifier : AIDSLINE MED/20351320
Raza A; Rush Cancer Institute, Rush-Presbyterian-St. Luke's Medical; Center, Chicago, Illinois 60612-3515, USA.araza@rush.edu
Abstract: An attempt has been made in this article to summarize the state-of-the-art clinical experience with the use of anti-TNF therapies in four diseased states with special emphasis on myelodysplastic syndromes. Given the central role of TNF-alpha in initiating and perpetuating the chronic damage produced in the diseased organs by controlling a cascade of pro-inflammatory cytokines, as well as its acute role in sepsis, theoretically speaking, neutralization of this peptide was a natural therapeutic choice. Results of the initial clinical trials appear encouraging and sometimes dramatic in their efficacy. The mechanism of response however, is interesting in that even when TNF-alpha is directly targeted by a monoclonal antibody, the resulting benefits can frequently not be attributed to TNF suppression alone. Rather, it appears that a more general effect on the T-lymphocytes is also contributing to the responses being seen. This raises the new possibility of combining anti-cytokine and anti-T-cell strategies to treat at least the more chronic diseases such as Crohn's disease and myelodysplastic syndromes. Continued clinical trials testing these strategies are clearly warranted. Copyright 2000 Wiley-Liss, Inc.
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