Tumour necrosis factor (TNF)-α and interleukin (IL)-17 are key cytokines driving psoriasis and other inflammatory autoimmune diseases, and thus represent effective targets for anti-psoriatic therapy. In a recent issue of The Journal of Pathology, Leite Dantas et al explore a mouse model of TNF-mediated psoriasiform dermatitis and arthritis with doxycyclin-inducible general overexpression of human TNF (ihTNFtg) mice for the contributions of macrophages and T cells in skin inflammation - with some unexpected and interesting findings. Although T cells are commonly known as major proinflammatory players in psoriasis, in the ihTNFtg mouse model macrophages were the predominant cells causing inflammation, and T cells, represented by Foxp3+ regulatory T cells, mainly formed the opposition to keep inflammation in check. In addition to offering a new perspective on potential alternative initiation mechanisms in psoriatic skin inflammation, this constellation illustrates how cellular networks in inflammatory conditions evolve according to the prevailing cytokine, and may help to explain individual responses to either anti-TNF-α or anti-IL-17 therapy regimens in psoriasis. Copyright © 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Keywords: T cell; TNF-α; Treg; biologicals; immune cell plasticity; inflammation; macrophage; psoriasis.
Copyright © 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.