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Lesions of IL-13−/ IL-13−/arrow chimeras displayed increased necrotic core formation, consistent with advanced plaque progression (Fig 6B).
Subsequent studies showed that VEGFR-1 signaling deficient bone marrow chimeras displayed a defect in monocyte migration leading to significant lower amount of myeloid cells in the tumor tissue [ 67].
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We are currently analyzing in vivo B cell responses of CD83mu B cells in wild-type/CD83mu bone marrow chimeras that display a normal T cell population due to T cell maturation on wild-type thymic epithelium.
WT/mdx∶utrophin−/− chimeras displayed a distinct phenotype from that of WT/mdx and thus, were named WT/mdx∶utrophin.
The rofA-containing chimera displayed a substantial increase in transcript abundance relative to wt Alab49.
Similarly, the BNAR chimera displayed the same binding specificity as Roc1b: it bound Cul3 but not Cul1 (Fig. 2B).
We observed comparable percentages of lymphocyte subpopulations in wild-type chimeras and mixed bone marrow chimeras (Figure S5A), indicating normal lymphopoiesis in mixed bone marrow chimeras.
Bone marrow chimeras were analyzed at 4 8 weeks post-bone marrow transfer (BMT).
Bone marrow chimeras were generated using the Ly5.1/5.2 reconstitution system, as previously described [6].
Using bone marrow chimeras, the cardioprotective role of PI3Kγ was mapped to non-haematopoietic cells.
In this report we used 4-1BB-deficient mice and bone marrow chimeras to address this issue.
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