NFKB2/p52 transgenic mice express an N terminal truncation of the NFKB2 protein in lymphocytes. Approximately 76% of 6-12 month old hemizygous mice develop inflammation in the lungs, salivary glands and kidneys.  Both spleen and lymph nodes sizes are increased.  Inflammation is characterized by an infiltration of lymphocytes (in particular, activated B cells and CD4+ T cells) and macrophages.  Serum from transgenic mice contains an 8.2 fold increase in anti-dsDNA autoantibodies as compared to wild-type.  Approximately half of the mice develop immune complex glomerulonephritis. Autoimmune disease in these mice appears to be a function of p52 down-regulation of  the pro-apoptotic protein BIM leading to defects in apoptosis of autoreactive lymphocytes. These mice may be useful for studies involving NFKB2 signaling pathways and autoimmunity.

NFKB2/p52 transgenic mice express an N terminal truncation of the NFKB2 protein in lymphocytes. Mice exhibit inflammation in the lungs, salivary glands and kidneys, and immune complex glomerulonephritis.  These mice may be useful for studies involving NFKB2 signaling pathways and autoimmunity.

This strain is hosted by NIH's MMRRC, which partners with JAX for the distribution of this and other strains. <b>For additional information and to purchase, please visit the MMRRC site.</b>