Psoriasis vulgaris lesions contain discrete populations of Th1 and Th17 T cells.

By M. Lowes, T. Kikuchi, J. Fuentes-Duculan, I. Cardinale, Lisa C. Zaba, Asifa Haider, E. Bowman, J. Krueger. Journal of Investigative Dermatology, 2008

1,116 citations recorded by the source corpus.

Subfields: Dermatology, Immunology

View Paper: https://www.semanticscholar.org/paper/94207218f56e6473d487157b0517efff0193d09f

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Dermatology

1. Frank O. Nestle
2. J. Krueger
3. M. Suárez‐Fariñas

In Immunology

1. J. Krueger
2. Frank O. Nestle
3. M. Lowes
4. M. Suárez‐Fariñas
5. A. Di Cesare
6. P. Di Meglio
7. M. Kaplan
8. P. Miossec

Citations in the corpus

• Imiquimod-Induced Psoriasis-Like Skin Inflammation in Mice Is Mediated via the IL-23/IL-17 Axis1 (2009, background): “Expression of IL-23 is increased in psoriasis lesional skin (20, 21), and increased numbers of Th17 cells are present (22).”
• Mast cells and neutrophils release IL-17 through extracellular trap formation in psoriasis (2011, background): “Psoriasis lesions contain increased amounts of IL-17 mRNA and increased numbers of Th17 cells (2, 10, 11).”
• Th17 cells: biology, pathogenesis of autoimmune and inflammatory diseases, and therapeutic strategies. (2012, background): “Interestingly, IL-22 mRNA expression returned to non-lesional levels upon treatment with cyclosporine, a conventional therapy for psoriasis.(85) Moreover, IL-22”
• The IL-23/Th17 axis in the immunopathogenesis of psoriasis. (2009, background): “Furthermore, modulation of IL-23 by cyclosporin A, UV therapy, and by biological agents has been correlated to the clinical benefit in psoriatic patients (Piskin et al., 2004; Gottlieb et al., 2005; Lowes et al., 2008; Haider et al., 2008b).”
• Psoriasis and systemic inflammatory diseases: potential mechanistic links between skin disease and co-morbid conditions. (2010, background): “It is characterized by expansion and activation of Th-1, Th-17, and Th-22 T cells, with production of associated cytokines such as interferon-g, tumor necrosis factor (TNF), IL-17, and IL-22 in the skin (Lowes et al., 2008; Nograles et al., 2009).”
• Immunology of Psoriasis (2014, background): “In contrast to T cells of healthy skin, psoriasis lesional T cells produce abundant IL-17 when activated ex vivo by anti-CD3/CD28 or PMA/ionomycin (66).”
• Effects of AIN457, a Fully Human Antibody to Interleukin-17A, on Psoriasis, Rheumatoid Arthritis, and Uveitis (2010, background): “Indeed, inhibition of p40, the shared subunit of IL-23 and IL-12, is effective in the treatment of psoriasis (22).”
• Brodalumab, an anti-interleukin-17-receptor antibody for psoriasis. (2012, neutral): “Oral retinoids 2 (5) 2 (5) 6 (15) 7 (18) 6 (14) 21 (13)”
• Circulating Th17, Th22, and Th1 Cells Are Increased in Psoriasis (2009, positive): “These cells and the cytokines produced by these cells are found in increased levels within skin affected by psoriasis (Chan et al., 2006; Wolk et al., 2006; Wilson et al., 2007; Zaba et al., 2007; Kryczek et al., 2008; Lowes et al., 2008; Harper et al., 2009).”
• Integrative responses to IL-17 and TNF-α in human keratinocytes account for key inflammatory pathogenic circuits in psoriasis. (2011, background): “The Th17/ IL-23 pathway is highly increased in psoriatic skin lesions (Lee et al., 2004; Lowes et al., 2008; Di Cesare et al., 2009) and is central to psoriasis pathogenesis, as genetic CCL20”