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The article presents comments of the author on the research paper "Successful Response in a Case of Severe Pustular Psoriasis After Interleukin-1b Inhibition," by researcher P. Skendros and collegues. It is noted that generalized pustular psoriasis has more recently been associated with the spectrum of so-called auto-inflammatory diseases (AIDs), hereditary conditions that feature recurrent fever as a hallmark of inappropriate activation of pro-inflammatory signalling.

The author comments on the article "Early- and late-onset psoriasis: a cross-sectional clinical and immunocytochemical investigation," by E. Theodorakopoulou and colleagues. Topics discussed include subtypes of chronic plaque psoriasis such as type I and type II psoriasis, the link of interleukins with early-onset psoriasis (EOP) and late-onset psoriasis (LOP), and the impact of T-cell infiltration for psoriasis

This article presents information on research papers related to dermatology published in various journals. The research paper "Expression of Haptoglobin in Human Epidermal Cells," states that haptoglobin (Hp) is the inhibitor that prevents functional transformation of langerhans cells (LC). Using in situ hybridization, researchers found Hp mRNA expression in normal human keratinocytes but not in normal human epidermal LCs. Another research paper "The Dynamics of Gene Expression of Interleukin-19 and Interleukin-20 and Their Receptors in Psoriasis," investigates mRNA expression of IL-19, IL-20 and their receptors' in the skin of 18 psoriasis patients before, during and after short term treatment with either calcipotriol or ciclosporin A. IL-20 and IL-19 mRNA levels were found 22 and 65 fold, respectively, upregulated in lesional compared with non-lesional psoriatic skin.

Background Schnitzler's syndrome (SchS) is an autoinflammatory disease characterized by a chronic urticarial rash, a monoclonal component and signs of systemic inflammation. Interleukin ( IL)-1β is pivotal in the pathophysiology. Objectives Here we investigated the cellular source of proinflammatory mediators in the skin of patients with SchS. Methods Skin biopsies of lesional and nonlesional skin from eight patients with SchS and healthy controls, and patients with cryopyrin-associated periodic syndrome ( CAPS), delayed-pressure urticaria ( DPU) and cold-contact urticaria ( CCU) were studied. We studied in vivo IL-1β, IL-17 and antimicrobial protein ( AMP) expression in resident skin cells and infiltrating cells. In addition we investigated the in vitro effect of IL-1β, IL-17 and polyinosinic-polycytidylic acid (poly: IC) stimulation on cultured epidermal keratinocytes. Results Remarkably, we found IL-1β-positive dermal mast cells in both lesional and nonlesional skin of patients with SchS, but not in healthy control skin and CCU, and fewer in CAPS. IL-17-positive neutrophils were observed only in lesional SchS and DPU skin. In lesional SchS epidermis, mRNA and protein expression levels of AMPs were strongly increased compared with nonlesional skin and that of healthy controls. When exposed to IL-1β, poly: IC or IL-17, patient and control primary human keratinocytes produced AMPs in similar amounts. Conclusions Dermal mast cells of patients with SchS produce IL-1β. This presumably leads to activation of keratinocytes and neutrophil influx, and further amplification of inflammation by IL-17 (from neutrophils and mast cells) and epidermal AMP production leading to chronic histamine-independent neutrophilic urticarial dermatosis. [ABSTRACT FROM AUTHOR]

Background Recent reports have revealed the therapeutic potential of cell-mediated immunity in neoplasms such as cutaneous squamous cell carcinoma ( SCC). Objectives To define the antigenic coexpression of regulatory T cells (Tregs) and plasmacytoid dendritic cells ( pDCs) and assess the CD8+/Foxp3+CD25+ cell ratio at peritumoral and intratumoral levels in order to investigate a correlation with the aggressiveness of SCC tumours. Methods We evaluated the content and distribution of Foxp3+CD25+ Treg and CD123+ pDC infiltration and assessed CD8+/Foxp3+CD25+ cell ratio at peritumoral and intratumoral levels in 40 SCCs (20 well-differentiated, G1; and 20 moderately to poorly differentiated, G2-G3) to investigate a correlation with their aggressiveness. We determined the profiles of Tregs and CD123+ cells; immunostained for CD4, CD8, CD123, interleukin (IL)-1 and transforming growth factor (TGF)-β1; and unequivocally double stained for Foxp3CD25. Results Peritumorally, CD4, CD8 and Foxp3 expression showed no difference between the two groups. CD123+ cells were fewer in G2-G3 ( P = 0·0005), while Foxp3+ CD25+ cells were more numerous ( P = 0·0005). The Foxp3+ CD25+/Foxp3+ ratio was higher in G2-G3 cases ( P = 0·0005), confirming the trend in this group of activated T lymphocytes towards total Treg Foxp3+ cells, while the CD8+/Foxp3+ CD25+ ratio was higher in G1 ( P = 0·0005). Intratumorally, CD4+ and CD8+ cells infiltrated G2-G3 ( P = 0·048) more than G1 ( P = 0·004), whereas almost all cells were CD123 negative. Regarding Foxp3 CD25, TGF-β1 and IL-10, they were less expressed in G1, whereas they were positive in G2-G3 ( P < 0·05). The CD8+/Foxp3+ CD25+ ratio was similar to that observed in peritumoral infiltration. Conclusions Our data suggest that intratumoral recruitment of Tregs, high expression of TGF-β1 and IL-10, almost negative CD123+, and a low CD8+/Foxp3+ CD25+ T-cell ratio may contribute to the aggressiveness of cutaneous SCC, as already evidenced for other solid tumours. [ABSTRACT FROM AUTHOR]

The article discusses aspects related to immunological role of interleukin 31 for treatment of itching including deposition of amyloid as the causative condition for pruritus. Topics discussed include increased expression of primary localized cutaneous amyloidoses (PLCA), cutaneous T-cell lymphomas (CTCL), and antibody nemolizumab.

Presents a letter to the editor about the article "Is the pathogenesis of Sweet's syndrome mediated by interleukin-I?" by researcher J.J. Going.

Presents a letter to the editor characterizing the role of interleukin in Sweet's syndrome, published in the February 1992 issue of the "British Journal of Dermatology."