The Il2rg tm1Wjl targeted mutation b is a complete null mutation in the gene encoding the interleukin 2 receptor gamma chain (IL2Rγ, homologous to IL2RG in humans).Due to the Prkdc scid mutation, however, the NSG strain shows high sensitivity to radiation, T-cell leakage, and increased incidence of thymic lymphoma formation as such, this strain cannot be used to predict clinical response to certain anticancer drugs, or for long-term transplantation studies. The phenotypic penetrance of Prkdc scid varies among inbred strain backgrounds, but the mutation is most effective at eliminating adaptive immunity on the NOD genetic background. Mice homozygous for the mutation have severely reduced numbers of mature T and B cells. Prkdc scid is a loss-of-function mutation in the mouse homologue of the human PRKDC gene, which encodes a protein that resolves DNA strand breaks that occur during V(D)J recombination in developing T and B lymphocytes. The Prkdc scid mutation a, commonly known as “scid” or “ severe combined immunodeficiency”, essentially eliminates adaptive immunity.The NOD/ShiLtJ background also contributes an allele of the Sirpa gene that renders the bone marrow niche very permissive to colonization by human hematopoietic stem cells. The genetic background, derived from inbred NOD mouse strain NOD/ShiLtJ, contributes reductions in innate immunity that include an absent hemolytic complement system, reduced dendritic cell function, and defective macrophage activity.
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