They chose inflammation as a field of medical research, in which human data are available and in which the mouse models seem to have a very good mechanistic resemblance to the human disease situation.
Phenotypically, most of the existing mouse models seem to be a mixture of OC and GS, including mice deficient in Scrib (Carnaghan et al., 2013; Murdoch et al., 2003), Aebp1 (Layne et al., 2001; Danzer et al., 2010), Bmp1 (Suzuki et al., 1996), and Tfap2a (Brewer and Williams, 2004b) (description summarized in Table 3).
However, recent publications made it clear that the type of mouse model seems to play a crucial role as they differ in extent and type of Aβ pathology [39,35].
Therefore, the G3 mTerc−/− mouse model seems more suitable than wild‐type aging mice to study the effects of telomere shortening on microglia.
Although many different animal models for FAS have been developed [ 90], the mouse model seems to correlate best to the effects of prenatal alcohol exposure observed in humans [ 91].
The preference for the rat compared to the mouse model seems mainly to be due to the rat's greater size which makes the operational procedures less difficult [ 5].
The relative ease with which protection is generated in mouse and guinea pig models seems to have limited predictive value for vaccine efficacy in NHPs, the 'gold standard' animal model for EBOV [ 52].
The MUC1 TG mouse tumor model seems to back up the idea of tolerance against MUC1 in humans, but the modifications of MUC1 glycosylation observed in human cancer cells were not taken into account in these studies.
Our study shows that in our mouse models, MCs seem to be an important regulator, inducing metastasis via the SCF/cKit axis.
