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Critical Reviews™ in Eukaryotic Gene Expression

Erscheint 6 Ausgaben pro Jahr

ISSN Druckformat: 1045-4403

ISSN Online: 2162-6502

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 1.6 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.2 The Immediacy Index is the average number of times an article is cited in the year it is published. The journal Immediacy Index indicates how quickly articles in a journal are cited. Immediacy Index: 0.3 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00058 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.33 SJR: 0.345 SNIP: 0.46 CiteScore™:: 2.5 H-Index: 67

Indexed in

Involvement of Different Genes Expressions during Immunological and Inflammatory Responses in Vitiligo

Volumen 27, Ausgabe 3, 2017, pp. 277-287
DOI: 10.1615/CritRevEukaryotGeneExpr.2017019558
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ABSTRAKT

Vitiligo is a condition of the skin distinguished by hypo-pigmentation. Etiology of this disorder is unknown, and several theories and mechanisms have been hypothesized. The inflammatory response in vitiligo is thought to be mediated by polymorphism in genes such as FOXP3, ACE, APE, GSTP1, TLR, SOD, CTLA-4, TAP/LMP gene cluster, etc. Theories including reactive oxygen species model, Nrf2–antioxidant response element (ARE) pathway, WNT pathway, tyrosinase activity, biochemical, molecular, and cellular alterations have been hypothesized to explain vitiligo pathogenesis. Melanosomal proteins are involved in antigen processing. The antigens are expressed to the T-cells in the form of peptides with HLA class II molecules. T-cells are activated in response to the discharge of co-stimulatory molecules such as LFA-3 as well as ICAM-1. An adaptive immune response is thus elicited, and the melanocytes eventually die or start malfunctioning and the skin undergoes hypo-pigmentation. IFN-γ is known to be a melanocyte inhibitor of paracrine origin; it is clearly involved in the early onset of symptoms of vitiligo disease. The surge in the IFN-γ levels mediates augmented expression of ICAM-1 molecule on the melanocytes, thereby establishing cytokine-mediated destruction of melanocytes. Mainly, mediators released by melanocytes and the functionality of keratinocytes decrease the disease activity. Such mediators include ET-1 as well as SCF, increase the pigmentation particularly when a patient is given with the UVB treatment. By scavenging ROS and screening UV radiation, melanin limits the damage caused to the cutaneous cells by UV radiation. Various immune responses play important roles in vitiligo.

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