Taste buds are assemblies of elongated epithelial cells, which are innervated by gustatory nerves that transmit taste information to the brain stem. Taste cells are continuously renewed throughout life via proliferation of epithelial progenitors, but the molecular regulation of this process remains unknown. During embryogenesis, sonic hedgehog (SHH) negatively regulates taste bud patterning, such that inhibition of SHH causes the formation of more and larger taste bud primordia, including in regions of the tongue normally devoid of taste buds. Here, using a Cre-lox system to drive constitutive expression of SHH, we identify the effects of SHH on the lingual epithelium of adult mice. We show that misexpression of SHH transforms lingual epithelial cell fate, such that daughter cells of lingual epithelial progenitors form cell type-replete, onion-shaped taste buds, rather than non-taste, pseudostratified epithelium. These SHH-induced ectopic taste buds are found in regions of the adult tongue previously thought incapable of generating taste organs. The ectopic buds are composed of all taste cell types, including support cells and detectors of sweet, bitter, umami, salt and sour, and recapitulate the molecular differentiation process of endogenous taste buds. In contrast to the well-established nerve dependence of endogenous taste buds, however, ectopic taste buds form independently of both gustatory and somatosensory innervation. As innervation is required for SHH expression by endogenous taste buds, our data suggest that SHH can replace the need for innervation to drive the entire program of taste bud differentiation.

The treatment of ACH is known to be difficult. Standard topical and systemic psoriasis therapies have been used to treat ACH, although the response is not consistent. 2,3 Furthermore, tumour necrosis factor-a antagonists have been employed with variable results in the treatment of ACH. [4][5][6][7] Efalizumab is a recombinant, humanized anti-CD11, a monoclonal immunoglobulin G1 antibody the use of which has been well documented in multiple, phase III, randomized, placebo-controlled, multicentre studies in the treatment of moderate-to-severe plaque psoriasis. 8,9 At the best of our knowledge, efalizumab has never been used in the treatment of ACH. However, it proved to be effective and did not cause any adverse effects in our patient. Even though more cases are needed to validate the efficacy of efalizumab in ACH, its use could represent a valid option in the limited array of treatment available for ACH.