A tale of two plaques: convergent mechanisms of T-cell-mediated inflammation in psoriasis and atherosclerosis.

Dermatology Clinical Research Unit, Teledermatology Program, Department of Dermatology, University of California, 3301 C St., Suite 1400, Sacramento, Davis, CA 95816, USA.
Experimental Dermatology (Impact Factor: 4.12). 07/2011; 20(7):544-9. DOI: 10.1111/j.1600-0625.2011.01308.x
Source: PubMed

ABSTRACT Psoriasis and atherosclerosis are diseases in which effector T lymphocytes such as Helper T cells type 1 (Th1) and 17 (Th17) play integral roles in disease pathogenesis and progression. Regulatory T cells (Treg) also exert clinically important anti-inflammatory effects that are pathologically altered in psoriasis and atherosclerosis. We review the immunological pathways involving Th1, Th17 and Treg cells that are common to psoriasis and atherosclerosis. These shared pathways provide the basis for mechanisms that may explain the epidemiologic observation that patients with psoriasis have an increased risk of heart disease. Improved understanding of these pathways will guide future experiments and may lead to the development of therapeutics that prevent or treat cardiovascular complications in patients with psoriasis.

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    ABSTRACT: In the last few years, a substantial body of evidence indicates that cutaneous psoriasis and psoriatic arthritis patients are at higher risk of developing cardiovascular disease. However, underlaying mechanism remains no completed understood. In this review we discuss the role of the immune system in the development of atherosclerosis, focusing on available data implicating the role of an enhanced immune-mediated pro-inflammatory status in psoriasis and psoriatic arthritis diseases.
    01/2015; 24. DOI:10.1016/j.ijcme.2015.01.005
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    ABSTRACT: Objectives Increased frequency of atrial fibrillation (AF) has been demonstrated in psoriasis cases. Prolongation of the duration of atrial electromechanical delay (AEMD) is a well-known characteristic of the atrium, which is vulnerable to AF. In the current study, our aims are to investigate AEMD durations and mechanical functions of the left atrium (LA) in patients with psoriasis.MethodsA total of 90 patients, 45 with psoriasis vulgaris and 45 as the control group, were included in the study. Atrial electromechanical coupling (PA) and intra- and inter-atrial electromechanical delay (IA-AEMD) were measured with tissue Doppler echocardiography. P-wave dispersion (PWD) was calculated from the 12-lead electrocardiogram. The severity of the disease was evaluated by the Psoriasis Area and Severity Index.ResultsThe durations of PA lateral and PA septal were significantly high in the psoriasis group when compared with the control group (47.7 ± 9.8 vs. 57.1 ± 8.4 msec, P < 0.001 and 38.6 ± 9.9 vs. 43.6 ± 8 msec, P = 0.016, respectively). The durations of IA-AEMD, intra-right electromechanical delay, and intra-left electromechanical delay in the psoriasis group were significantly prolonged compared with the control group (15.2 ± 4.1 vs. 21.7 ± 5.6 msec, P < 0.001; 6 ± 2.5 vs. 8.7 ± 2.7 msec, P < 0.001; and 9.1 ± 3.9 vs. 13.5 ± 5.2 msec, P < 0.001; respectively). PWD was significantly higher in patients with psoriasis vulgaris compared with controls (36.1 ± 7.9 vs. 40.2 ± 9.1 msec, P = 0.043).Conclusion In the present study, we found prolongation in the durations of AEMD and PWD in the psoriasis group compared with the control group. These results might be an early predictor of AF and other arrhythmias.
    Echocardiography 08/2014; 32(4). DOI:10.1111/echo.12706 · 1.25 Impact Factor
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    ABSTRACT: Psoriasis is a common chronic inflammatory skin disease that results from interplay between the immune system and the epithelium. In light of the very successful anti-cytokine therapies for psoriasis, the focus has been directed towards the adaptive immune system. Expression studies, genetic studies and treatments specifically targeting players of the IL-23/IL-17 pathway, point at an important role for IL-17 in the pathogenesis of psoriasis. IL-17 stimulates the keratinocytes to produce psoriasis-associated molecules, eventually leading to chronic skin inflammation.The current opinion is that IL-17 is mainly produced by T cells, so-called T helper 17 (Th17) cells, in psoriasis. However, evidence is accumulating that cells of the innate immune system, like neutrophils, mast cells, γδ T cells and innate lymphoid cells are the main source of IL-17 in psoriasis, rather than T cells. The paradigm in this field of research is shifting. With this viewpoint article we will address this novel concept by critically summarizing the current literature on this subject.In psoriatic arthritis and atherosclerosis, important conditions related to psoriasis, it was also found that the majority of IL-17 is associated with cells of the innate immune system. This new concept changes our view of IL-17. Blocking IL-17 with targeted treatments might be more far-reaching than previously thought. not only IL-17 production by T cells but also by innate immune cells is blocked. Furthermore, therapies specifically targeting IL-17 may not only improve psoriasis, but also comorbidity that is associated with the IL-17 pathway, hereby preventing serious complications on the long term.This article is protected by copyright. All rights reserved.
    Experimental Dermatology 07/2014; DOI:10.1111/exd.12487 · 4.12 Impact Factor

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