Inbred mice strains are key tool in scientific research being genetically identical and homozygous. There are many developed standard mice strains used for different purposes and research topics. In the Laboratory of Experimental Immunology a couple of different mouse strains are sustained, including healthy and predisposed to diseases breeds.
BALB/cJ is a commonly used inbred. Key traits include a susceptibility to certain infectious agents; widely used in cancer research, including spontaneous reticular neoplasms, primary lung tumors, and renal tumors. BALB/c mice injected with the mineral oil pristane develop lupus-like syndrome and are convenient model for studying autoimmunity.
SCID (severe combined immunodeficiency disease ) mice are homozygous for Prkdc-scid allele coding for DNA repair complex protein. This defective allele leads to impaired VDJ rearrangement that causes B and T cells deficiency. These mouse are ideal for xenoengraft transfer of human cells and tissue reducing the risk of these cells being rejected. They are also used for tumor growth studies and studies of normal and abnormal lymphocyte development and function.
NSG SCID gamma (129S4-Rag2tm1.1Flv Il2rgtm1.1Flv/J)
NSG mice are extremely immunodeficient, as they carry two mutations on the NOD/ShiLtJ genetic background: severe combined immune deficiency (scid) and a complete null allele of the IL-2 receptor common gamma chain (IL2rg-null). The scid mutation is in the DNA repair complex protein Prkdc and renders the mice B and T cell deficient. The IL2rg-null mutation prevents cytokine signaling through multiple receptors, leading to a deficiency in functional NK cells. The severe immunodeficiency allows the mice to be humanized by engraftment of human CD34+ hematopoietic stem cells (HSC), peripheral blood mononuclear cells (PBMC), patient derived xenografts (PDX), or adult stem cells and tissues. The immunodeficient NSG mice enable research in human immune function, infectious disease, diabetes, oncology, and stem cell biology.
MRL/lpr (MRL/MpJ-Fas<lpr>/J C)
MRL-lpr mice are homozygous for the lymphoproliferation spontaneous mutation (Fas-lpr), and show systemic autoimmunity, massive lymphadenopathy associated with proliferation of aberrant T cells, arthritis, and immune complex glomerulonephritis. These mice are useful as an autoimmunity model to determine the etiology of systemic lupus erythematosus (SLE) and Sjorgren (Sicca) syndrome and to evaluate therapies.
C57BL/6J are one of the most commonly used strains. Popular in wide array of research areas, including cardiovascular biology, developmental biology, diabetes and obesity, genetics, immunology, neurobiology, and sensorineural research.
The NOD/ShiLtJ strain (Non-obese Diabetic; commonly called NOD mice) is a polygenic model for autoimmune type 1 diabetes. Diabetes in NOD mice is characterized by hyperglycemia and insulitis and leukocytic infiltration into the pancreatic islets. Immune phenotypes in the NOD background consist of defects in antigen presentation, T lymphocyte repertoire, NK cell function, macrophage cytokine production, wound healing, and C5 component of the complement system.
Zbtb20 mutant mice
Zbtb20 deficient/mutant mice are produced on the 129/Sv genetic background. The BTB zinc finger gene Zbtb20 encodes a transcription factor belonging to the POK (Poxviruses and Zinc-finger (POZ) and Krüppel) family of transcriptional repressors. Homozygous Zbtb20 KO animals are viable at birth, but display dwarfism and die during the first month of postnatal life. Zbtb20 is critical for the formation of the central nervous system and its pathogenesis can contribute to neurological disorders.