The innate immune response may have been the major contributor to the inflammation associated with anaemia in these mouse strains since suppression of T cells with CsA had no observable effect.
Irwin et al. (Irwin et al., 2014) show that the differential activity of clofazimine in BALB/c and C3HeB/FeJ mice is specifically related to the granulomatous pathology in the lungs of these mice, and not due to differences in immune function between mouse strains, since clofazimine is also effective in immunocompromised, interferon-γ knockout mice.
Since expression of Cre recombinase does not result in lethality in other conditional mouse strains, and since the Jackson Laboratory currently has another Tek-Cre mouse strain in development, which is stated to be viable as Tek homozygotes, we suggest that this lethality originates from the site of insertion of the Tek-Cre transgene, which may disrupt the function of an essential gene.
Although the list of strains that were discussed in Götz and Ittner (2008) is long, it is still incomplete, since a myriad of AD and FTD mouse strains has been generated since the early 1990s and it is impossible to present them all.
Both insulin and IGF1 seem to play a role in mammalian aging, since mouse strains with reduced IIS show lifespan extension [ 5].
This effect depended on the correlation between temperature and body fat responses, since mouse strains with a lower reduction in T b under CR also had a lower reduction in body fat, suggesting CR life-extending responses are associated with minimal loss of temperature and least reduction in body fat (Liao et al. 2011).
The different genetic background also can have a large effect on physiological processes, since different mouse strains show different sensitivities to neurodegenerative influences (see [24] for a discussion of genetic background effects).
Whilst these data were suggestive of genetic determination of GTM profiles, further analyses was necessary to differentiate between environmental and genetic factors, since individual mouse strains were housed together with like strains and familial GTM profiles could be perpetuated through maternal contact and by coprophagia.
It is, however, possible to use all 3 mouse strains in these homing experiments since the time span examined are relatively short as to avoid an immune response from the immune competent mice towards the xenotransplanted EOCs.
Direct in vivo evidence for the interaction of BAT3/NKp30 for the recognition and elimination of tumor cells remains difficult since NKp30 is a pseudogene in mouse strains [38].
Since the xenograft models utilize immune deficient mouse strains to avoid graft rejection, immunologic microenvironments of transplanted GBM cells can be specifically modified by choosing a recipient mouse strain with defined immune deficiency status.
