TNF and psoriasis: Several key mechanisms have been proposed as initiating and maintaining psoriasis, including the activation of dendritic cells by complexes of self-DNA and the antimicrobial peptide cathelicidin LL-37, the presentation of putative auto-antigens to T lymphocytes, and the release of pro-inflammatory mediators such as interleukin (IL)-23, tumor necrosis factor-α (TNF-α) and IL-17A, leading to the activation of keratinocytes, which close the loop by producing antimicrobial peptides such as LL-37, chemoattractants and β-defensins 1–3.