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The same seems to be true in mouse mesenchymal stem cells (mMSCs) C3H10T1/2.
This seems to be true in mouse models of Mycobacterium tuberculosis in which low-dose priming induces highly sensitive T cells that can make a broad cytokine response that is associated with protection [ 55].
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That seems to be true in mice, at least.
Previous work indicates that anaemia in humans is associated with a reduction in plasma S1P levels without a change in RBC-associated S1P, suggesting that total RBC S1P 'capacity' influences plasma S1P levels in humans, although the same may not be true in mice [ 14, 22, 25].
What is true in mice is often not true in humans; results routinely defy common-sense assumptions and therapies based on incomplete knowledge can cause more harm than good.
In humans, stem cells renew at a higher rate in the large intestine compared to the small, while the opposite is true in mice.
The same is true in mice in which invariant natural killer T-cells, Paneth cells and even granulocytes can produce IL-17A [ 14].
This was also found to be true in a mouse-rat comparison relative to rodent specific segmental duplications [ 9].
This can also be true in humanized mice, in which human genetic variants have been introduced in an artificial genetic interactive environment.
The latter appears to be true in human and mouse, at least under pathological conditions such as neurodegeneration, schizophrenia and alcohol addiction [ 15, 23- 25].
In humans, the CD27+ memory B cell population contains the majority of antigen-experienced B cells [23], [24], and we reasoned that the same should be true in vaccinated HIS mice.
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