Mice homozygous for the Faslgld mutation display lymphadenopathy and systemic autoimmunity similar to that in Faslpr homozygous mice. There is significant enlargement of all lymph nodes, an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes, and these mice develop immune complex glomerulonephrosis.Read More +
Mice homozygous for the Faslgld mutation display lymphadenopathy and systemic autoimmunity similar to that in Faslpr homozygous mice. There is significant enlargement of all lymph nodes to 50 times the control weight by 20 weeks of age. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis. Onset of symptoms is dependent on genetic background with the C3H/HeJ strain having the earliest onset exhibiting glomerulonephritis by 22 weeks. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
|Allele Name||generalized lymphoproliferative disease|
|Allele Synonym(s)||CD95-; FasL-; gld; Tnfsf6gld|
|Gene Symbol and Name||Fasl, Fas ligand (TNF superfamily, member 6)|
|Strain of Origin||C3H/HeJ|
|Molecular Note||A T-to-C transition point mutation near the 3' end of the coding sequence causes a replacement of a highly conserved phenylalanine with a leucine at position 273 (p.F273L) in the extracellular region of the encoded protein.|
When using the CPt.C3-Faslgld/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #002932 in your Materials and Methods section.