However, despite the obvious benefits of murine models (including experimental simplicity, small size, familiarity, ease of husbandry and relative low costs), these differences mean that these animals do not faithfully model the clinical situation in DMD: therapeutic trials can be hard to assess in mildly affected mdx mice and are difficult to interpret in double-mutant mice [18].
Spontaneous genetically lupus-prone murine models including NZBWF1/J (NZB/W), MRL/MpJ-Faslpr/J (MRL-lpr), and congenic lupus strain B6.MRL-Faslpr/J (B6-lpr) have been extensively used in numerous published reports and have provided valuable insight into lupus pathogenesis.
For example, Helicobacter hepaticus, a potential pathogenic microorganism that has been reported to induce colitis, hepatitis, and hepatocellular carcinoma in numerous murine models including A/JCr, SCID/NCr and RAG-2−/− mice failed to induce colitis or to potentiate colitis in conventionalized IL-10−/− mice [24].
Therefore, TCDD treatment in vivo suppresses autoimmune inflammation in several murine models including EAE [ 13, 14], UC [ 15], experimental autoimmune uveoretinitis (EAU) [ 122], and type 1 diabetes [ 123].
Overall, this highlights that the use of diet intervention in murine models, including the use of humanized gnotobiotic mice, can mimic the changes in gut microbiota that occur in relation to human diet.
CP-690550 doses/exposures that produced effects in this model are consistent with those demonstrating immune suppression in other murine models including delayed-type hypersensitivity and cardiac allograft transplantation [ 5, 6].
Other murine models include mice with a combined knock out of TP53 and the gene encoding p18INK4c, which results in the development of angiosarcomas as well as other cancers of soft tissue (Harvey et al., 1993; Zindy et al., 2003).
Requirements for an appropriate murine model include a close resemblance to the pathology of the disease in humans, the objective measurement of the physiologic parameters, as well as reliability and reproducibility of the experimental data.
Shared characteristics of infection of heart tissue among these cases and our murine model include mixed inflammatory infiltrates [ 31, 33, 40], and myocyte necrosis [ 33, 40], with random inflammatory foci found throughout heart tissue.
Several forms of murine genetic models, including SHR, have become the focus of hypertensive research.
In several murine cancer models including chemically and genetically induced primary lung tumors, prostate tumors, colon xenografts, and lung metastases, TAMs expressed M2 early during tumorigenesis [ 6].
