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. Author manuscript; available in PMC: 2019 Mar 1.
Published in final edited form as: Nat Immunol. 2018 May;19(5):421–425. doi: 10.1038/s41590-018-0084-4

Table 1.

The challenges created by the illusion of similarity

The paradox Mouse Human
Fibrosis and IBD Fibrotic lesions such as those seen in CD are rarely observed in mouse models of IBD Fibrosis and strictures are a common occurrence in CD
IL-17 and IBD IL-17 has been shown to be deleterious or protective Antibody to IL-17 exacerbates inflammatory bowel disease
Phenotype of immune cells T cells from mice exposed to conventional microbiota resemble T cells from neonatal humans Mature T cell phenotype in humans observed only in mice colonized with complex microbiota
Clinical signs of infections Mice fail to develop the clinical signs seen in humans after infection with H. pylori, C. difficile or influenza virus H. pylori, C. difficile and influenza virus each produce a distinct disease in humans
LPS Mice relatively resistant to LPS Humans very sensitive to LPS

In these representative examples of differences between animal models and human disease, some heterogeneity could reflect technical limitations of genetic deletions that might not mimic specific alleles, whereas others might reflect environmental differences that affect microbiota or fundamental differences with evolutionary roots. H. pylori, Helicobacter pylori; C. difficile, Clostridium difficile; LPS, lipopolysaccharide.