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The RAGxCγ double mutant mice lack mature T cells, B cells, and functional NK cells, and are deficient in cytokine signaling, leading to better engraftment of human cells than any other published mouse strain [34].
These mice, in addition to lacking mature B and T cells, have reduced levels of NK cells compared to NOD/scid mice [27].
Previous experiments have shown that Rag1-deficient mice, lacking mature B and T cells, could not be rescued from lethal ECTV infection by cotreatment with MVA [8], [9].
In vivo, Rag1-/ mice lacking mature lymphocytes did not exhibit any bone phenotype, but lost their bone mass after ovariectomy like KΔ75 mice.
We then address the role played by mature lymphocytes in normal osteoclastogenesis and in bone physiology, analyzing Rag1-/ mice lacking mature B and T lymphocytes, concomitantly with KΔ75 and double mutant Rag1-/- KΔ75 mice.
To generate viable Relb-deficient mice, these were bred with Tcra-deficient mice, which do not express the αβ T-cell receptor (TCR) and therefore lack mature T cells.
Two categories of antigens can activate B cells, and they are defined as T-cell independent or T-cell dependent antigens based on their ability to induce antibodies in athymic (nude) mice that lack mature T cells [24].
It has been shown that VEGF secreted from pericytes can also contribute to vessel stabilization [24], and vessels lacking mature pericytes are prone to regression in the hyperoxia model [25].
