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The bovine system shows many similarities to the well-characterised human and murine systems, with a couple of exceptions.
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In this respect, the murine system, with the many available immunological reagents and knockout strains may provide the best system to identify these host sensors.
Behboudi et al. reported that rMVA induces DC dysfunction in the murine system with stimulation of MHC class I down-regulation and apoptosis [28], whereas Drillien et al. demonstrated moderate activation of human DCs by MVA [29].
Recently, several laboratories have established that mast cells have a critical role in the pathogenesis of synovitis in a murine system with considerable similarity to rheumatoid arthritis (RA) [ 1, 2].
However, these studies were performed with overexpression of mutant FLT3 in murine systems.
Two studies in the human system and several studies in murine systems have approached the question of whether DC function changes with aging and how this affects immune-competence.
In murine systems AHR activation can directly affect the differentiation and innate immune functions of inflammatory DCs without affecting their ability to interact with T cells [ 42, 43].
Knowledge of factors that regulate HSC activity is derived largely from murine model systems, with serial transplantation often considered a "gold standard" to assess longevity and self-renewal of HSCs.
The advantage of the LLC model is that implanted cells are immunologically compatible with the murine system, unlike the widely used xenograft models in which human cells are implanted into mouse tissue.
These results agree closely with studies in the murine system that showed hyporesponsiveness to TLR stimulation after Francisella infection [49], [50].
This finding, together with our results in the murine system, is a strong argument against TiA as a major factor of resistance against NK cells.
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