New Concepts in the Pathogenesis of Psoriasis

Twenty years ago, a concept of psoriasis pathogenesis was proposed in which epidermal proliferation of psoriatic lesions was the consequence of immunological abnormalities. This concept has subsequently been supported by the remarkable efficacy of immunosuppressive drugs. Moreover, recent experimental data indicate that activated psoriatic lymphocytes are capable of inducing keratinocyte proliferation. However, we have still to explain the mechanism by which lymphocytes act on keratinocytes and to find out what antigenic material could be responsible for their activation.

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Immunopathogenesis of Psoriasis: News in an Old Concept

Guilhou

1998

“…Much attention has been directed to the influence of cytokines in psoriasis [2, 3]and it is considered to be an auto-immune disease [4, 5, 6]. A defective response of the hypothalamus-pituitary-adrenal axis to cytokine stimuli was suggested as a possible site of abnormality in inflammatory auto-immune diseases [7, 8].…”

Section: Introductionmentioning

confidence: 99%

Prolactin: Does It Have a Role in the Pathogenesis of Psoriasis?

Giasuddin¹,

El-Sherif

El-Ojali³

1998

Background: The aetiopathogenesis of psoriasis is still not fully understood. Recently, it has been reported that prolactin (PRL) exerts a proliferative effect on human keratinocytes in vitro. PRL may, therefore, play an important role in the pathogenesis of psoriasis. Objective: To assess the serum PRL level in patients with psoriasis vulgaris (PV). Methods: Serum levels of PRL were estimated in 12 patients with PV (age: 11–45 years with mean ± SD 30.4 ± 10.2 years; sex: 7 males, 5 females) and the results were compared with those in 9 patients with atopic dermatitis (age: 15–47 years with mean ± SD 28.1 ± 11.9 years; sex: 4 males, 5 females) and 20 normal control subjects (age: 16–45 years with mean ± SD 36.1 ± 11.9 years; sex: 15 males, 5 females). Results: Serum PRL in PV (mean ± SD 25.8 ± 16.1 ng/ml) was significantly higher compared to those in atopic dermatitis (mean ± SD 9.1 ± 4.7 ng/ml) and normal control subjects (mean ± SD 10.3 ± 5.3 ng/ml; ANOVA → p = 0.0008). Three patients with PV (2 males and 1 female with ages of 35, 40 and 11 years, respectively) had the highest serum levels well above the normal range but they were <100 ng/ml, the minimum limit for the diagnosis of prolactinoma (χ² test → p <0.025). Conclusion: Since PRL belongs to the growth hormone family, its raised serum level may have a role in the hyperproliferation of kerationocytes in vivo, the hallmark of the psoriasis disease process.

“…A possible role of HERVs (or slow viruses) in psoriasis has already been proposed [1, 45] and was subsequently supported by several experimental observations. The early morphological studies showing virus-like particles in psoriatic patients were intriguing but remained questionable [46,47,48].…”

Section: Search For Human Endogenous Retrovirusesmentioning

confidence: 52%

“…The disease is clinically and histologically well characterized in its common presentation and associates proliferation and abnormal differentiation of keratinocytes with immune disturbances closely related to autoimmunity [1, 2]. Although the interplay between keratinocytes and the immune cells is better understood, the origin of psoriasis remains unknown.…”

Section: Introductionmentioning

confidence: 99%

New Hypotheses in the Genetics of Psoriasis and Other ‘Complex’ Diseases

Guilhou¹,

Molès²

2008

Psoriasis is a complex genetic disorder in which the disease, according to the current concept, is caused by the interplay of many different genes. However, recent genetic studies indicate that the location of these genes varies considerably among populations and families, raising the question of how the same phenotype can be induced by such variable genetic linkages. To circumvent these discrepancies we propose that psoriasis could be induced by the same repetitive DNA sequence, an endogenous retroviral element present at different locations in the genome. The occurrence of the disease could be linked to an abnormal activation of one or more endogenous retroviral element copies due to their location and/or to modification of their sequence. This unifying concept would simplify our understanding of genetically complex diseases.