Common clinical features and disease mechanisms of psoriasis and psoriatic arthritis

Myers, W. A.; Opeola, Mobolaji; Gottlieb, Alice B.

doi:10.1007/s11926-004-0043-y

Cited by 18 publications

(8 citation statements)

References 30 publications

(27 reference statements)

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“…9,10 Moreover, the damaged keratinocytes might produce more cytokines that recruit more immunocytes. 11 The gradual increase in B cell count from non-tumorigenic, to pre-tumorigenic, and finally to tumorigenic lesions go in line with other groups. 5,6 Also, Perez et al (1999) reported that the intensity of MICs increases with the promotion/progression stages during squamous carcinogenesis (AK → SCC).…”

Section: Discussionsupporting

confidence: 71%

Analysis of the mononuclear inflammatory cell infiltrate in the nontumorigenic, Pretumorigenic and tumorigenic keratinocytic hyperproliferative lesions of the skin

Hussein¹,

Ahmed²

2005

Cancer Biology & Therapy

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Background: The keratinocytic hyperproliferative lesions include non-tumorigenic, pre-tumorigenic (actinic keratoses, AK), and tumorigenic (squamous cell carcinomas, SCC) conditions. Although mononuclear inflammatory cell infiltrate (MICs) is a constant feature in these lesions, their immunophenotypic characterization is still incomplete. We hypothesized that the development of non-tumorigenic, pre-tumorigenic, and tumorigenic keratinocytic hyperproliferative lesions is associated with alterations in the mononuclear inflammatory cell infiltrate in response to altered antigenicity of the lesional cells. This study tries to test this hypothesis and to characterize MICs in these lesions.Methods: Fifty lesions (non-tumorigenic lesions, 29; AK, 9 and SCC, 12) were examined using immunoperoxidase staining methods and antibodies targeting histiocytes (CD68), T cells (CD3), B cells (CD20), and T cells with cytotoxic potential (TIA-1).Results: As compared to the normal skin, the development of the keratinocytic hyperproliferative lesions (normal skin; non-tumorigenic; AK and SCC) was associated with a statistically significant increase(p = <0.05) in: (1) CD20 + B lymphocytes (0.0 ± 0.0 vs. 3.1 ± 0.5 vs. 7.5 ± 0.3 vs. 14.5 ± 5.5); (2) CD68 histiocytes (4.0 ± 1.0 vs. 26.5 ± 3.9 vs. 23 ± 1.9 vs. 41.3 ± 6.8); (3) CD3 + T lymphocytes (3.0 ± 1.1 vs. 58.3 ± 10.3 vs. 54.5 ± 0.2 vs. 41.0 ± 16.0); and (4) TIA-1 + cytotoxic T cells (1.8 ± 0.4 vs. 2.9 ± 0.7 vs. 9.6 ± 1.1 vs. 13.7 ± 5.2).Conclusions: The increase in the number of infiltrating mononuclear cells in all pathologic lesions compared to normal skin may reflect increased antigenicity of the lesional cells. Both humoral and cell mediated immunity are involved in these lesions.

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Section: Discussionsupporting

confidence: 71%

Analysis of the mononuclear inflammatory cell infiltrate in the nontumorigenic, Pretumorigenic and tumorigenic keratinocytic hyperproliferative lesions of the skin

Hussein¹,

Ahmed²

2005

Cancer Biology & Therapy

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“…Thirdly, the clinical benefit of PUVA (psoralen combined with UVA) therapy is in part due to the impairment of T-cell function [55]. Fourthly, psoriasis can be associated with other T-cell-mediated immune diseases, such as inflammatory bowel diseases and coeliac disease [56][57][58]. Fifthly, in vitro studies show that lesional skininfiltrating CD4 + T-cells release factors that increase keratinocyte proliferation [59].…”

Section: T-cells As Mediators Of Skin Inflammation In Psoriasismentioning

confidence: 99%

Psoriasis: from pathogenesis to novel therapeutic approaches

et al. 2010

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Psoriasis is one of the commonest chronic inflammatory disorders. Its cause is unknown, but a wealth of studies indicate that the disease results from a complex and dynamic interplay between genetic and environmental factors that trigger an excessive inflammatory response in the skin. Dendritic cells and effector T-cells are central in the development of the psoriastic lesion, and cytokines produced by these cells stimulate keratinocytes to proliferate and increase the migration of inflammatory cells into the skin, promoting epidermal hyperplasia and inflammation. Understanding the immunology of the psoriatic plaque has led to new therapeutic options and novel candidates for immunomodulation, and has changed the ways psoriatic patients are managed.

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“…Psoriasis is a hereditary and chronic inflammatory skin disorder affecting 2-3% of the Caucasian population [53]. It is mediated by T cells, dendritic cells and inflammatory cytokines and characterized by marked increases in keratinocyte proliferation, prominent alterations in dermal capillary vasculature [54].…”

Section: Psoriasismentioning

confidence: 99%

Arterial Distensibility in Chronic Inflammatory Rheumatic Disorders

Yıldız¹

2010

TOCMJ

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Abstract:The pulse wave velocity (PWV), as an indicator of arterial distensibility, may play an important role in the stratification of patients based on the cardiovascular risk. PWV inversely correlates with arterial distensibility and relative arterial compliance. Decreased arterial distensibility alters arterial blood pressure and flow dynamics, and disturbes coronary perfusion. Systemic immune and inflammatory diseases, such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) are associated with increased morbidity and mortality, predominantly due to adverse cardiovascular events. Systemic inflammation in these disorders may alter arterial compliance and arterial distensibility and, through this effect, lead to accelerated atherosclerosis. We have demonstrated an increase in the carotid-femoral (aortic) PWV that is a technique in which large artery elasticity is assessed from analysis of the peripheral arterial waveform, in patients with chronic inflammatory conditions such as RA, SLE, familial Mediterranean fever (FMF), Wegener's granulomatosis (WG), sarcoidosis, psoriasis and psoriatic arthritis except Behçet's disease (BD). In this review, the issue of arterial stiffness in RA, SLE, as well as WG, psoriasis, FMF, BD, sarcoidosis, systemic sclerosis (SS) and Takayasu's arteritis (TA) is overviewed.

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Common clinical features and disease mechanisms of psoriasis and psoriatic arthritis

Cited by 18 publications

References 30 publications

Analysis of the mononuclear inflammatory cell infiltrate in the nontumorigenic, Pretumorigenic and tumorigenic keratinocytic hyperproliferative lesions of the skin

Analysis of the mononuclear inflammatory cell infiltrate in the nontumorigenic, Pretumorigenic and tumorigenic keratinocytic hyperproliferative lesions of the skin

Psoriasis: from pathogenesis to novel therapeutic approaches

Arterial Distensibility in Chronic Inflammatory Rheumatic Disorders

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