T cell responses to heat shock proteins (HSP) have disease suppressive activities through production of anti-inflammatory cytokines in patients and in models of inflammatory diseases. There is evidence that the anti-inflammatory activity of HSP-specific T cells depends on their recognition of endogenous HSP epitopes as expressed by stressed cells at sites of inflammation. Previously, we have demonstrated that such T cells can be induced by conserved sequences of microbial HSP. Now we propose that drug induced up-regulation of endogenous HSP can contribute to anti-inflammatory T cell regulation.