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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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The Goldilocks Conundrum: NLR Inflammasome Modulation of Gastrointestinal Inflammation during Inflammatory Bowel Disease

Volumen 36, Ausgabe 4, 2016, pp. 283-314
DOI: 10.1615/CritRevImmunol.2017019158
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ABSTRAKT

Recent advances have revealed significant insight into inflammatory bowel disease (IBD) pathobiology. Ulcerative colitis and Crohn's disease, the chronic relapsing clinical manifestations of IBD, are complex disorders with genetic and environmental influences. These diseases are associated with the dysregulation of immune tolerance, excessive inflammation, and damage to the epithelial cell barrier. Increasing evidence indicates that pattern recognition receptors, including Toll-like receptors (TLRs) and nucleotide-binding domain and leucine-rich repeat-containing proteins (NLRs), function to maintain immune system homeostasis, modulate the gastrointestinal microbiome, and promote proper intestinal epithelial cell regeneration and repair. New insights have revealed that NLR family members are essential components in maintaining this immune system homeostasis. To date, the vast majority of studies associated with NLRs have focused on family members that form a multiprotein signaling platform called the inflammasome. These signaling complexes are responsible for the cleavage and activation of the potent pleotropic cytokines IL-1β and IL-18, and they facilitate a unique form of cell death defined as pyroptosis. In this review, we summarize the current paradigms associated with NLR inflammasome maintenance of immune system homeostasis in the gastrointestinal system. New concepts related to canonical and noncanonical inflammasome signaling, as well as the implications of classical and alternative inflammasomes in IBD pathogenesis, are also reviewed.

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