| A very similar story can be told about Denise Faustman's ongoing research into the cure. She has also cured Type I in mice, although using other means. And she also got her share of first-class controversy.
Cf. http://www.diabeteshealth.com/read/2005/05/01/4126/why-did-t... and the preceding New York Times article "I BEG TO DIFFER; A Diabetes Researcher Forges Her Own Path to a Cure" http://bit.ly/bzUkWs . The JDRF doens't look good in this case at all. More information about her approach at http://www.faustmanlab.org/ A good overview of other immune-based therapeutic approaches from 2006 can be found at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1868847/ It's interesting to follow the scientific debate. The 2006 review sponsored by JDRF claims that the methods used by Faustman offer little promise, and can even be harmful. She offers a completely opposite view, claiming in a 2008 paper Because our findings showing potential benefits of TNF
or TNF agonism for treating AI, it seems paradoxical
that anti-TNF therapies are a major therapeutic class
of drugs currently marketed for AI. TNF antagonists
have provided clinical benefit to about half of AI patients,
those with rheumatoid arthritis and Crohn's disease. Yet an
expanding body of research in animal models on spontaneous
autoimmunity suggests the opposite strategy may be
warranted. Furthermore, in humans, several clinical
observations deserve mention. First, many Crohn's and
rheumatoid arthritis patients never respond to TNF
antagonists. Second, long-term treatment with anti-TNF drugs
can be accompanied by onset of new or aggravated forms of
autoimmunity, sometimes new autoantibodies, suggesting that,
for some AIs, anti-TNF therapy may not be the drug of choice .
(http://www.pnas.org/content/105/36/13644.full)To me, the JDRF arguments sound more fishy than hers. It's a tricky business of solving puzzles like that, especially as an outsider. But it's fun to see how far one can go following the debate. |