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However, IgE is not the only factor governing FcεRI expression, since mast cells from IgE-deficient (IgE−/−) mice express low levels of FcεRI [30].
Mast cells from IgE deficient mice express low levels of FcεRI [28] which suggests that the basal levels are under the control of other regulators.
These mice express low levels of peptide-empty MHC class I molecules, which can however be stabilized at the cell surface by the addition of exogenuous peptide [37].
Although the WTTg mice express low levels of αB-crystallin, they are distinct from KOTg mice, which are devoid of αB-crystallin since embryogenesis.
Mast cells from IgE deficient mice express low levels of FcεRI unless up-regulated by in vitro incubation of these cells with IgE or injection of IgE in vivo [28].
In line with our results, a recent report shows that T cells from p110δ−/− mice express low GzmB when activated with anti-CD3ε but, in contrast to our data, antitumor T cell responses were impaired (Putz et al., 2012).
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Genetically modified mice expressing low levels of F3 exhibited reduced IL-6 expression and increased survival during endotoxemia (Pawlinski and Mackman 2004).
Interestingly, IL-33 expression levels in the RPE cells were strain dependent, while RPE cells in C57BL/6 mice expressed low levels of IL-33 (Fig. 2C and E), the expression was higher in the RPE cells of nonpigmented BALB/c mice (Fig. 2D and F).
In summary, we generated transgenic mice expressing low amounts of R122H mutated human cationic trypsinogen.
In addition, CTLs from B6 and TLR-2-/ mice expressed low levels of TLR-4.
CD11c+ IDO+ DCs from tolerized mice expressed low levels of MHC II and CD86, suggesting an immature phenotype.
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