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Critical Reviews™ in Immunology

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ISSN Druckformat: 1040-8401

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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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The Human Immune System against Staphylococcus epidermidis

Volumen 39, Ausgabe 3, 2019, pp. 151-163
DOI: 10.1615/CritRevImmunol.2019031282
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ABSTRAKT

Staphylococcus epidermidis is one of the major causes of nosocomial infections in humans. This organism can exist as a commensal on the skin. However, it can also lead to severe infections. The immune system has evolved mechanisms to deal with microorganisms and has strategies to combat bacteria. The initial defense against S. epidermidis infections includes the activation of complement complex, recruitment and then killing of the microorganism by effectors. The success of pathogenic S. epidermidis strains has been attributed to their capacity to evade innate immune cells. Extracellular matrix binding protein, polysaccharide intercellular adhesin, and accumulation-associated protein have been found to suppress killing of S. epidermidis by effector cells. PSM constitutes the only kind of exported toxins in S. epidermidis strains and has strong cytolytic features against leukocyte cells. The human innate immune system can be stimulated against S. epidermidis via toll-like receptors that enhance antibacterial reactions, trigger inflammation, and result in the stimulation of immune system effectors, e.g., type-1 interferon (IFN-alpha and IFN-beta), proinflammatory cytokines, and nitric oxide. Proinflammatory cytokines, e.g., interleukin-1, interleukin-6, and tumor necrosis factor are formed from resident human cells and result in migration of the lymphocyte and fever. In this review we will examine the immune system's response against S. epidermidis.

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