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Pristane-treated granzyme B-deficient mice also produced antibodies directed against the U1-70-kd antigen, a previously identified granzyme B substrate.
Primary cultures of microglial cells of APOE4 transgenic mice also produced significantly more nitric oxide than microglia from APOE3 transgenic mice.
Isolated LPMCs from TLR2−/− mice also produced greater than 7-fold more IL-17A compared to WT cells when restimulated with anti-CD3e and anti-CD28 (p<0.001) (Figure 6E).
All mice also produced USDs.
F1 APP and PS1 heterozygous mice also produced multiple litters (Fig. 1B, F2).
In addition, peritoneal phagocytic cells from TLR4-dysfunctional C3H/HeJ mice also produced IL-12 upon uptake of OMLs.
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Mitochondria from the liver and brain of ovariectomized mice also produce more H2O2 [23].
Hsf1 −/− female mice also produce defective oocytes that, when fertilized, do not develop very far into embryogenesis [16].
PD-1−/− mice also produce increased levels of inflammatory cytokines such IL-17, which should be protective, yet due to the concomitant increase in IL-4 production, these mice are unable to control the bacterial burden.
Furthermore, a corroborating study showed that MSCs obtained from mice also produce adenosine to suppress T-cell proliferation [ 51].
Stromal fibroblasts isolated from COX-2 deficient, but not COX-1 deficient, mice also produces far less (>90%) VEGF than fibroblasts from wild-type mice [ 87].
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