I am writing in response to a letter from Gericke et al. commenting on our paper recently published in The Journal of Immunology. In that paper we showed that 9-cis-retinoic acid was capable of inhibiting the NF-κB-mediated induction of TSLP gene expression. The main point of the paper was that this inhibition, which had been first postulated by Lli et al. (1), was actually an indirect effect on the activation of NF-κB, and not a direct effect on the TSLP promoter. Gericke et al. in their letter refer to data in a manuscript in preparation, which we have not seen, and therefore cannot comment on, that the data are suspect because we did not use RXR- or RAR-selective agonists. They also state that they could replicate our observations, although no details were provided as to the experiments they performed. While we agree that our studies would have benefited from selective agonists (we have recently shown that all-trans retinoic acid can also inhibit NF-κB-mediated TSLP gene expression), this point does not detract in any respect from the general conclusion of the paper: that the effect of these agonists on TSLP gene expression is indirect through inhibition of NFκB activation.

Li, M., N. Messaddeq, M. Teletin, J. L. Pasquali, D. Metzger, P. Chambon.
. Retinoid X receptor ablation in adult mouse keratinocytes generates an atopic dermatitis triggered by thymic stromal lymphopoietin.
Proc. Natl. Acad. Sci. USA