Anti-TNF therapies in rheumatoid arthritis, Crohn's disease, sepsis, and myelodysplastic syndromes

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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‐α 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‐α 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. Microsc. Res. Tech. 50:229–235, 2000.