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operate through up-regulation of the immune system. In both seemingly
opposite therapeutic regimes, the key molecular-level interactions are
likely to be the same; the tannin binds (competitively with the lipid A
segment of LPS) at the lipid A receptor complex, and either induces or
suppresses further signal transduction, depending upon the structural
details of the tannin construct. Much refinement of this preliminary and
necessarily crude mechanistic picture will be a first step toward realizing
the goal of a clinically useful tannin-inspired therapeutic agent in either
the antitumor or the anti-sepsis fields.
Acknowledgements
We gratefully acknowledge funding from the National Institutes of
Health, Institute of General Medical Science (GM72572).
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