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In line with these findings, using a mouse strain lacking Nampt expression in the T and B cell lineage, Rongavaux and colleagues have recently shown that Nampt is critically required for the development of both T and B lymphocytes [9].
The mdx mouse strain, lacking a functional dystrophin gene, has served as the animal model for human DMD (2).
Another murine model for human PBC is a knockout mouse strain lacking the interleukin 2 receptor, α chain (IL2Rα) gene.
A cohort of male congenic Friend virus B-type (FVB) mouse strain lacking β2-adrenoceptor (β2KO) (Chruscinski et al. 1999) and their age-matched FVB wild type (WT) controls at 2 months of age were used in this study.
Results: Through establishing an arthritis model by injecting arthritogenic serum into wild-type and NADPH oxidase 2 (NOX2 -deficient mice, we fouNOX2 -deficientis had a neutrophilic infiltrate and was mice severe in Ncf1 −/− mice, a mouse strain lacking the expression of the NCF1/p47phox component of NOX2.
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IGFBP3 and Epo have both been shown to support endothelial cell survival and mouse strains lacking these factors displayed increased hyperoxia-induced vessel loss [46], [47].
Injection of muscarinic antagonists in distinct brain regions cause pronounced augmentation in locomotor activity levels [32], [33], [35] and a hyperactivity phenotype was observed in mouse strains lacking M1 and M4 muscarinic receptors [30], [31], [52] as well as mouse strains null for the nicotinic β2 receptor [29], [36], [37].
Therefore, it is unlikely that Fas-FasL induced apoptosis plays an important role in elimination of mature T cells, which might account for the low rates of T cell reconstitution and T cell numbers in our control mice or other similar humanized mouse strains lacking expression of HLA-DR4 molecules.
In particular, experimental studies demonstrate effects of CNIs in mouse strains lacking an adaptive immune system, so their findings cannot be attributed to CNI suppression of T-cell immunity.
Two mouse strains lacking p600 (p600−/−) were found to be embryonic lethal between E9.5 and E14.5 (depending on the strain, genetic background, and individual variation) with abnormal development of several embryonic tissues (including microcephalic brain) and extra-embryonic organs (yolk sac, placenta) and an overall growth defect (Nakaya et al., 2013; Tasaki et al., 2013).
Modeling this loss-of-function syndrome in mice recapitulates the human pain-free phenotype; acute thermal and mechanical insults have no behavioral consequences, whereas inflammatory pain is also abolished in inbred mouse strains lacking Nav1.7 in peripheral neurons (Minett et al., 2012, Nassar et al., 2004).
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