Because the IL-17 axis is known to be essential for psoriasis induction in these models [21], the relative resistance of the TCRδ−/− mice was attributed to their lack of dermal IL-17-producing γδ T cells rather than to their lack of DETC, since Imiquimod treatment induces dermal γδ T cells but not DETC to produce copious amounts of IL-17. The gene discussed is IL17A; the disease is psoriasis.