Lipocalin-2 exacerbates psoriasiform skin inflammation by augmenting T-helper 17 response.
Tokyo, Japan. In J Dermatol, Jan 2016
Clinically, i.p. injected LCN2 exacerbated erythema and scaling in IMQ-treated murine skin compared with phosphate-buffered saline injection alone, and it augmented interleukin (IL)-17A, IL-17F, IL-22, IL-23p19, IL-12p40, CCL20, tumor necrosis factor-α, chemokine (C-X-C motif) ligand (CXCL)1, CXCL2, DEFB4, DEFB14, LCN2 and S100A7 mRNA levels of IMQ-treated murine skin while it did not increase the mRNA levels of interferon-γ, IL-12p35 or CXCL10.
Genetics of psoriatic arthritis.
St. John's, Canada. In Best Pract Res Clin Rheumatol, 2014
Searching for different types of genetic variants such as small CNVs and/or insertions/deletions has also led to the identification of several genes with a function relative to PsV in particular including DEFB4, LCE3C_LCE3B, and IL-22 gene (exon 1).
The pathogenesis and genetics of psoriasis.
Barcelona, Spain. In Actas Dermosifiliogr, 2014
Most of these genes can be incorporated into an integrated pathogenic model of psoriatic disease comprising distinct signaling networks affecting skin barrier function (LCE3, DEFB4, GJB2), innate immune responses involving nuclear factor-κB signaling (TNFAIP3, TNIP1, NFKBIA, REL, FBXL19, TYK2, NOS2, CARD14), and adaptive immune responses involving CD8 T cells and interleukin 23 (IL-23)/IL-17-mediated lymphocyte signaling (HLA-C, IL12B, IL23R, IL23A, TRAF3IP2, ERAP1).
München, Germany. In J Mol Med (berl), 2005
Recently, two novel human beta-defensins, human beta-defensin-3 (HBD-3), and human beta-defensin-4 (HBD-4) have been discovered.