Immunopathological characterization of selected mouse models of inflammatory bowel disease: Comparison to human disease
Pathophysiology, ISSN: 0928-4680, Vol: 21, Issue: 4, Page: 267-288
2014
- 50Citations
- 116Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations50
- Citation Indexes50
- 50
- CrossRef49
- Captures116
- Readers116
- 116
Review Description
Inflammatory bowel diseases (IBD) are chronic, relapsing conditions of multifactorial etiology. The two primary diseases of IBD are Crohn's disease (CD) and ulcerative colitis (UC). Both entities are hypothesized to occur in genetically susceptible individuals due to microbial alterations and environmental contributions. The exact etiopathogenesis, however, is not known for either disease. A variety of mouse models of CD and UC have been developed to investigate the pathogenesis of these diseases and evaluate treatment modalities. Broadly speaking, the mouse models can be divided into 4 categories: genetically engineered, immune manipulated, spontaneous and erosive/chemically induced. No one mouse model completely recapitulates the immunopathology of CD or UC, however each model possesses particular similarities to human IBD and offers advantageous for specific details of IBD pathogenesis. Here we discuss the more commonly used models in each category and critically evaluate how the immunopathology induced compares to CD or UC, as well as the advantages and disadvantages associated with each model.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0928468014000273; http://dx.doi.org/10.1016/j.pathophys.2014.05.002; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84912562037&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/24935242; https://linkinghub.elsevier.com/retrieve/pii/S0928468014000273; https://dx.doi.org/10.1016/j.pathophys.2014.05.002
Elsevier BV
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