PEER-REVIEW | DERMATOLOGY |
Figure 1 Gene expression of IL-17 in psoriatic lesions
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The level of gene expression of IL-17 in psoriatic lesions in comparison with non-lesion skin. The results were normalized to the GAPDH gene.
inflammatory tissues, including fibroblasts,
chondrocytes, osteoblasts, mast cells, neutrophils, and epithelial cells in vessels and skin12
. Psoriasis and atherosclerosis are inflammatory
diseases, so an increase of IL-17 expression in atherosclerotic lesion vessels and psoriasis skin lesions indicates the key role the Th17 cells play in these diseases.
The IL-17 triggers
synthesis of IL-6 in fibroblasts, which activate and differentiate the native T-cells to Th17, which leads to the generation of a positive feedback and the support of an inflammatory reaction to Th17 in both diseases.
The IL-17 stimulates keratinocytes and epithelial cells
of vessels to produce CXC chemokine: CXCL1, CXCL5, CXCL8, attractants of neutrophils and CCL20, which attracts CCR6+ cells to the inflammation area13
. References
1. Volkov, VI Pro-inflammatory cytokines, and soluble intracellular adhesion molecules in coronary heart disease. Wolves Cardiology 2002; 9: 12–16
2. Titov VN, Lisitsyn D, Tvorogova MG. Correlation of hypercholesterolemia and blood levels of double bonds of the polyene fatty acids. Klin Lab Diag 1999; 9: 28
3. Austin LM, Ozawa M, Kikuchi T, Walters IB, Krueger JG. The majority of epidermal T cells in Psoriasis vulgaris lesions can produce type 1 cytokines, interferon-gamma, interleukin-2, and tumor necrosis
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factor-alpha, defining TC1 (cytotoxic T lymphocyte) and TH1 effector populations: a type 1 differentiation bias is also measured in circulating blood T cells in psoriatic patients. J Invest Dermatol 1999; 5(113): 752–9
4. Weigle N, McBane S. Psoriasis. Am Fam Physician 2013; 87(9): 626–633
5. Gonzalez-Juanatey C, Llorca J, Amigo-Diaz E, Dierssen T, Martin J, Gonzalez-Gay MA. High prevalence of subclinical atherosclerosis in psoriatic arthritis patients without clinically evident cardiovascular disease or classic atherosclerosis risk factors. Arthritis Rheum 2007;
6(57): 1074–80
6. Gu C, Wu L, Li X. IL-17 family: cytokines, receptors and signaling. Cytokine 2013; 64: 477–485
7. Rouvier E, Luciani MF, Mattei MG, Denizot F, Golstein P. CTLA-8, cloned from an activated T cell, bearing AU-rich messenger RNA instability sequences, and homologous to a herpesvirus saimiri gene. J Immunol 1993; 54: 5445–5456
8. Madhur MS, Funt SA, Li L, Vinh A, Chen W, Lob HE, Iwakura Y, Blinder Y, Rahman A, Quyyumi AA, Harrison DG. Role of interleukin 17 in inflammation, atherosclerosis, and vascular function in apolipoprotein
e-deficient mice. Arterioscler Thromb Vasc Biol 2011; 7(31): 1565–72
9. Livak K, Schmittgen T. Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. Methods. 2001; 25(4): 402–8
10. Aggarwal S, Ghilardi N, Xie MH, de Sauvage FJ, Gurney AL. Interleukin-23 promotes a distinct CD4 T cell activation state characterized by the production of interleukin-17. J Biol Chem 2003; 3(278): 1910–4
11. Witowski J, Ksiazek K, Jorres A. Interleukin-17: a mediator of inflammatory responses. Cell Mol
Life Sci 2004; 5(61): 567–79
12. Paunovic V, Carroll HP, Vandenbroeck K, et al. Signalling, inflammation and arthritis: crossed signals: the role of interleukin (IL)-12, -17, -23 and -27 in autoimmunity. Rheumatol 2008; 47 (6): 771–6
13. Harper EG, Guo C, Rizzo H, et al. Th17 cytokines stimulate CCL20 expression in keratinocytes in vitro and in vivo: Implications for psoriasis pathogenesis J. Invest Dermatol 2009; 129: 2175–83
14. Yao Z, Painter SL, Fanslow WC, et al. Human IL-17: A novel cytokine derived from T cells. J Immunol 1995; (155): 5483–6
7 8 9 10 Key points The increased
expression of the IL-17 gene in affected vessels and psoriatic lesions confirms a major role of the IL-17 family in the initiation and progression of inflammatory diseases
IL-17 is involved in
molecular mechanisms of atherogenesis and psoriasis and performs an inflammatory action within many processes
A high IL-17 gene
expression level of can represent the pathological processes in psoriasis and atherosclerosis and indicate the effectiveness of treatment at the molecular level
The level of gene expression of IL-17 in atherosclerotic vessels compared to unaffected parts of the femoral artery.
The IL-17 triggers synthesis of IL-6 in fibroblasts, which
activate and differentiate the native T-cells to Th17, which leads to the generation of a positive feedback and the support of an inflammatory reaction to Th17 in both diseases14
. In all likelihood, the IL-17 involved in the molecular
mechanisms of atherogenesis and psoriasis performs the inflammatory role in many processes, such as cell adhesion, blood cell movement in tissue, activation cells, and T-cell (co)stimulation/ proliferation, as well as the presentation of antigens in the inflammatory cascade for atherosclerosis and psoriasis.
Therefore, it is possible to assume that a high-level expression of the IL-17 gene can represent the
pathological process in psoriasis and atherosclerosis and indicates the effectiveness of treatment at the molecular level.
Declaration of interest None
Figure 2 Gene expression of IL-17 in atherosclerotic vessels
1000 p <0.05 100 10 0 1 2 3 4 5 6 PATIENT 7 8 9 10
August/September 2015 |
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