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Critical Reviews™ in Immunology

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ISSN Druckformat: 1040-8401

ISSN Online: 2162-6472

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: 1.3 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: 2.6 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: 0.00079 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: 0.24 SJR: 0.429 SNIP: 0.287 CiteScore™:: 2.7 H-Index: 81

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Identifying Crosstalk between Raf Kinase Inhibitor Protein and Systemic Lupus Erythematosus

Volumen 39, Ausgabe 6, 2019, pp. 423-437
DOI: 10.1615/CritRevImmunol.2020033377
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ABSTRAKT

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease in which hyperactive autoantibodies attack and damage healthy tissues and organs. SLE can affect multiple organs, such as the skin, kidneys, joints, and brain. The pathogenesis of SLE is multifaceted and complex, making it difficult to develop targeted therapies to ameliorate symptoms and the onset of disease. A number of signaling pathways have been investigated and shown to be implicated in SLE; however, information regarding the specific pathways involved, at least in part, in the pathogenesis of SLE remains scarce. The role of Raf kinase inhibitor protein (RKIP) in key signaling pathways in cancer is well-studied. However, studies highlighting the role of RKIP in autoimmune diseases and the inflammatory response are emerging. Whereas the induction of RKIP in cancer is associated with improved responses and reduced resistance, the overexpression of RKIP in normal tissues inhibits inflammatory cytokines and chemokines and may also inhibit autoimmunity. In this review, we have analyzed the potential crosstalk between the signaling pathways that regulate SLE and RKIP and whether targeting the pathways that activate the expression of RKIP may prove to be a novel therapeutic tool against the pathogenesis of SLE.

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