Characterization of Mononuclear Cell Infiltrates in Psoriatic Lesions

Bjerke, J R; Krogh, H.K.; Matre, R.

doi:10.1111/1523-1747.ep12529841

Cited by 105 publications

(41 citation statements)

References 28 publications

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“…In psoriasis, the typical epidermal changes include hyperproliferation and incomplete terminal differentiation [8, 9], whereas dermal changes include an infiltration of immunocompetent cells mainly of mononuclear origin [8, 10, 11]. Topical corticosteroids and vitamin D 3 analogues are effective antipsoriatic treatments.…”

Section: Introductionmentioning

confidence: 99%

Decrease in Enkephalin Levels in Psoriatic Lesions after Calcipotriol and Mometasone Furoate Treatment

Nissen

Avrach²,

Hansen³

et al. 1999

Dermatology

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Background: Enkephalins are opioid peptides that can modulate immune responses and inflammatory processes. Furthermore, they inhibit keratinocyte proliferation/differentiation in vitro. Previously, we have shown that enkephalins are present in increased amounts in lesional psoriasis. Objective: To determine the effect of topical treatment with the vitamin D analogue calcipotriol and the corticosteroid mometasone furoate on the level of methionine-enkephalin (enk) in psoriatic lesions. Methods: Twelve psoriatic patients were treated with calcipotriol and mometasone furoate for 14 days without or with hydrocolloid occlusion. Keratome biopsies were obtained from treated and untreated skin, and the extracted enk was quantified by radioimmunoassay. Furthermore, punch biopsies were obtained for immunohistochemical analysis. Results: Clinically, both calcipotriol and mometasone furoate improved psoriasis to the same degree, the effects being more pronounced after occlusion. Histologically, treatment with mometasone furoate without occlusion decreased both the epidermal thickness/parakeratosis and the number of dermal immunocompetent cells (CD3- and CD68-positive cells). In contrast, treatment with calcipotriol without occlusion reduced the epidermal thickness and the degree of parakeratosis but decreased the number of CD3- and CD68-positive cells only slightly. The mean enk level was decreased by 26 and 86% by calcipotriol without and with occlusion and by 16 and 63% by mometasone furoate without and with occlusion, respectively. The decreases in the enk levels corresponded to the degree of clinical improvement but not to the histological changes. Conclusion: The increased levels of enk in psoriatic lesions are reduced in parallel with the clinical improvement induced by a topical vitamin D analogue and a corticosteroid. Because enkephalins can modulate epidermal differentiation and inflammatory processes, the findings indicate that enkephalins may play a role in the pathogenesis of psoriasis.

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Section: Introductionmentioning

confidence: 99%

Decrease in Enkephalin Levels in Psoriatic Lesions after Calcipotriol and Mometasone Furoate Treatment

Nissen

Avrach²,

Hansen³

et al. 1999

Dermatology

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“…However, after the discovery that immunosuppressive agents are effective in psoriasis therapy, it is now considered to be an immune-mediated disease [65]. Inflammatory infiltrates appear early in the psoriatic lesions, even before the epidermal changes can be observed [66]. The over-expression of pro-inflammatory cytokines is considered to be responsible for the initiation, maintenance and recurrence of psoriatic skin lesions.…”

Section: Inflammatory Featuresmentioning

confidence: 99%

Psoriasin For Better or for Worse in Sickness and in Health : The Role of Psoriasin in Angiogenesis and Differentation of Epithelial Cells

Vegfors¹

2014

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-I - ABSTRACTPsoriasin (S100A7), a member of the S100 family of calcium-binding proteins, is highly expressed in high-grade ductal carcinoma in situ (DCIS) and in the benign hyperproliferative skin disorder psoriasis. Both breast cancer and psoriasis are diseases which are characterized by hyperproliferation and a disturbed differentiation of the epithelial cells as well as a pronounced angiogenesis. The potential role of psoriasin in angiogenesis and the epithelial cell differentiation remain unclear.The aim of this thesis was to investigate the cellular effects of psoriasin in angiogenesis and the differentiation processes, with special emphasis on breast cancer and psoriasis.We found that psoriasin expression was induced in mammary epithelial cells and keratinocytes by oxidative stress. Psoriasin expression was shown to induce vascular endothelial growth factor (VEGF) expression and several other pro-angiogenic factors in epithelial cells. Upon down-regulation of psoriasin, H2O2-induced expression of VEGF was decreased as well as the pro-angiogenic factors heparin-binding EGF-like growth factor (HB-EGF) and matrix metalloproteinase (MMP)-1. Extracellular psoriasin contributed to the subsequent induction of proliferation, migration and tube formation of endothelial cells. The proliferative effect of psoriasin was shown to be mediated by the receptor for advanced glycation end products (RAGE). Furthermore, psoriasin induced reactive oxygen species (ROS) in both endothelial and epithelial cells through the action of RAGE, and contributed to the expression of the proangiogenic factors in endothelial cells.The expression of psoriasin was up-regulated in mammary epithelial cells and keratinocytes in response to differentiation-inducing stimuli and was shown to be regulated by pathways involved in epithelial cell differentiation. Upon psoriasin down-regulation the shift towards a more differentiated CD24+-phenotype of mammary epithelial cells was abolished. Furthermore, the expression of the differentiation markers involucrin, desmoglein 1, transglutaminase 1 and CD24 was decreased in keratinocytes upon down-regulation of psoriasin expression. ABSTRACT -II -In vivo we demonstrated a gradient of psoriasin expression in the psoriatic epidermis, with intense expression in the suprabasal differentiated layers, and a similar staining pattern between psoriasin and the differentiation marker CD24 in DCIS tumors.In conclusion, our findings describe psoriasin as a mediator in the angiogenic process and a contributor of epithelial cell differentiation. Consequently, psoriasin is possibly a contributor to the development and progression of breast cancer and psoriasis and a potential target in the treatment of these diseases. POPULÄRVETENSKAPLIG SAMMANFATTNING -III - POPULÄRVETENSKAPLIG SAMMANFATTNING BETYDELSEN AV PROTEINET PSORIASIN FÖR NYBILDNINGEN AV BLODKÄRL OCH UTMOGNADEN AV CELLER FÖR UTVECKLINGEN AV BRÖSTCANCER OCH PSORIASISBröstcancer är den vanligaste cancerformen bland kvinnor. I likhet med andra cancersjukd...

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“…Evidence of the pivotal role played by T-cells in the pathology of psoriasis is accumulating, such as • presence of activated T-cells in psoriatic lesions (Bjerke et al 1978) • the ability of activated T-cells to induce the altered keratinocyte growth and differentiation pattern typical of psoriasis, as demonstrated in the so-called psoriasis SCID mouse model: Injection of autologous immunoctyes into non-lesional skin grafts from psoriatic donors onto mice with a severe combined immune defi ciency results in the phenotype of lesional psoriatic skin (Nickoloff and Wrone-Smith 1999) • effi cacy of T-cell-targeted immune suppressive drugs, such as cyclosporine, and antibodies against the CD25 receptor and CD4 (Schön and Boehncke 2005) • transfer of psoriasis in the process of bone marrow transplantation from a donor suffering from the disease to a healthy recipient (Gardembas-Pain et al 1991). Also, psoriasis can be "cured" when bone marrow is transplanted from a healthy donor to a person with psoriasis (Eedy et al 1990).…”

Section: The Role Of T-cells In the Pathogenesis Of Psoriasismentioning

confidence: 99%

Efalizumab in the treatment of psoriasis

Boehncke

2005

Journal of the American Academy of Dermatology

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Abstract:The humanized antibody efalizumab is currently the only T-cell directed biologic approved for the treatment of moderate-to-severe psoriasis by both American and European authorities. Binding to and blocking the function of the adhesion molecule leukocyte function associated antigen 1 (LFA-1), it is believed to interfere with T-cell activation in the lymph node, migration through the circulation into the skin, and re-activation in-loco, all of these representing central steps in the pathogenesis of psoriasis. A comprehensive clinical development program provided large and consistent evidence that efalizumab induces a major clinical benefi t in psoriasis. Efalizumab rapidly and substantially improves psoriatic skin symptoms and leads to profound gain in quality of life. It allows safe and effective long-term control of psoriasis. Therefore, evidence-based treatment guidelines recommend its use in moderate to severe plaque-type psoriasis.

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Characterization of Mononuclear Cell Infiltrates in Psoriatic Lesions

Cited by 105 publications

References 28 publications

Decrease in Enkephalin Levels in Psoriatic Lesions after Calcipotriol and Mometasone Furoate Treatment

Decrease in Enkephalin Levels in Psoriatic Lesions after Calcipotriol and Mometasone Furoate Treatment

Psoriasin For Better or for Worse in Sickness and in Health : The Role of Psoriasin in Angiogenesis and Differentation of Epithelial Cells

Efalizumab in the treatment of psoriasis

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