• Publications
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Pathogenesis and therapy of psoriasis
The newest therapies for psoriasis target its immune components and may predict potential treatments for other inflammatory human diseases. Expand
Immunology of psoriasis.
The genetic background of psoriasis and its relationship to immune function, specifically genetic mutations, key PSORS loci, single nucleotide polymorphisms, and the skin transcriptome are discussed. Expand
Increased Expression of Interleukin 23 p19 and p40 in Lesional Skin of Patients with Psoriasis Vulgaris
The data suggest that IL-23 is playing a more dominant role than IL-12 in psoriasis, a Th1 type of human inflammatory disease. Expand
Psoriasis vulgaris lesions contain discrete populations of Th1 and Th17 T cells.
Th17 cells may be proximal regulators of psoriatic skin inflammation, and warrant further attention as therapeutic targets, and suggest that psoriasis is a mixed Th1 and Th17 inflammatory environment. Expand
Brodalumab, an anti-interleukin-17-receptor antibody for psoriasis.
Bdalumab significantly improved plaque psoriasis in this 12-week, phase 2 study and was superior to placebo in all comparisons. Expand
Th17 cytokines interleukin (IL)‐17 and IL‐22 modulate distinct inflammatory and keratinocyte‐response pathways
This data indicates that suppression of Th1 and Th17 cytokines in Psoriasis vulgaris is a pro-inflammatory disease and the relative contribution of interferon, IFN,γ, interleukin and IL‐22 on disease pathogenesis is still unknown. Expand
The immunologic basis for the treatment of psoriasis with new biologic agents.
  • J. Krueger
  • Medicine
  • Journal of the American Academy of Dermatology
  • 2002
Critical steps in immunologic activation include Langerhans cell maturation (activation), T-cell activation, differentiation and expansion of type 1 T cells, selective trafficking of activated T cells to skin, and induction of an inflammatory cytokine and chemokine cascade in skin lesions. Expand
IL-22-producing "T22" T cells account for upregulated IL-22 in atopic dermatitis despite reduced IL-17-producing TH17 T cells.
It is established that T cells could independently express IL-22 even with low expression levels of IL-17, which argues for a functional specialization of T cells such that "T17" and "T22" T-cells may drive different features of epidermal pathology in inflammatory skin diseases. Expand
Integrative responses to IL-17 and TNF-α in human keratinocytes account for key inflammatory pathogenic circuits in psoriasis.
The data predict that Psoriasis therapy with either TNF or IL-17 antagonists will produce greater modulation of the synergistic/additive gene set, which consists of the most highly expressed genes in psoriasis skin lesions. Expand
Amelioration of epidermal hyperplasia by TNF inhibition is associated with reduced Th17 responses
It is shown that etanercept has early inhibitory effects on a newly appreciated type of T cells: T helper type 17 (Th17) cells, which may be particularly important in driving epidermal activation in psoriatic plaques whereas Th1 cells must also be eliminated for final disease resolution. Expand