Psoriasis pathogenesis and the development of novel targeted immune therapies
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347 citations
Cites background from "Psoriasis pathogenesis and the deve..."
...The effects of IL-17 on epidermal keratinocytes produce a feed-forward inflammatory response by activating C/EBPb and d, STAT1, and NF-kB, which amplify the primary signals driving the development of mature psoriatic plaques (24)....
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269 citations
Cites background from "Psoriasis pathogenesis and the deve..."
...This might explain why targeting specifically IL-23 through blockade of the p19 subunits represents a promising therapeutic option, even in a scenario dominated by anti-IL-17A treatments (44)....
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Cites background from "Psoriasis pathogenesis and the deve..."
...Perhaps equally important, such therapies have taught us a lot about disease mechanisms (1, 2)....
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...Clin Exp Immunol (2014) 176(2):266–74....
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...J Invest Dermatol (2014) 134(2):415–22....
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References
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"Psoriasis pathogenesis and the deve..." refers background in this paper
...IL-17 also acts synergistically with TNF to potentiate IL-17–induced transcription of several proinflammatory genes (eg, TNF, IL-1b, IL-6, and IL-8),47-50 which activate mDCs and promote the differentiation of T17 cells in the skin and draining lymph nodes.32,51 Epidermal hyperplasia, a hallmark of psoriatic plaques, is associated with STAT3 activation and indirectly regulated by J ALLERGY CLIN IMMUNOL SEPTEMBER 2017 648 HAWKES, CHAN, AND KRUEGER IL-17 through induction of IL-19 and/or IL-36 by keratinocytes.46 The increased proliferation of epidermal keratinocytes is likely further potentiated by IL-22 and possibly IL-20 because both of these cytokines are also activators of STAT3....
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...The increased proliferation of epidermal keratinocytes is likely further potentiated by IL-22 and possibly IL-20 because both of these cytokines are also activators of STAT3.(52,53) This marked thickening of the rapidly proliferating epidermis is accompanied by retention of the keratinocyte nucleus (parakeratosis), as well as upregulation of IL-17–induced transcription factors (eg, C/EBPb or C/EBPd) and keratinocyte-derived gene products, such as S100A7/8/9, hBD2, lipocalin-2, and CCL20....
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1,628 citations
"Psoriasis pathogenesis and the deve..." refers background or result in this paper
...Psoriasis autoantigens In a recent study of 56 patients, Lande et al(26) found that peripheral blood in 75% of patients with moderate-to-severe psoriasis contained autoreactive CD4(1) or CD8(1) T cells against LL-37/ cathelicidin, a cationic antimicrobial peptide (AMP) produced by keratinocytes and other immune cells (eg, neutrophils) in response to bacterial/viral infections(27,28) or skin trauma.(29) The cytokine profile of these autoreactive T cells revealed increased levels of skin-homing receptors (eg, cutaneous lymphocyte antigen, CCR6, and CCR10) and a strong IFN-g and IL-17 phenotype consistent with previous studies examining the T-cell...
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...Importantly, the authors also showed that LL-37 expression is upregulated in psoriatic plaques, correlates with disease activity, and results in direct activation of plasmacytoid dendritic cells (pDCs) and myeloid dendritic cells (mDCs) by forming a complex with nucleic acids (DNA and RNA) released after skin trauma.(29,31) These multimeric LL-37–nucleic acid complexes are protected from enzymatic degradation and enter dendritic cells (DCs) by way of specific Toll-like receptors....
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