Abstract

TNF inhibitors have been recently applied to treat psoriasis with great therapeutic efficacies. It has been demonstrated that TNF inhibitors attenuate psoriasis through down-regulation of the Th17 signals, but the underlying mechanism remains to be fully understood. TNF-α is processed from a membrane-bound form by TNF-αconverting enzyme (TACE) so that soluble TNF-αexerts its biological activity. Other than TNF-α, EGFR ligands, including heparin-binding EGF-like growth factor (HB-EGF), amphiregulin and transforming growth factor (TGF)–α are TACE substrates and are also recognized as psoriasis-associated growth factors.

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