Several of the papers that I've read recently using the EAE mouse model have made reference to the SJL/J mouse. Below is a description of the SJL/J phenotype provided by
Jackson Laboratories. The description is particularly interesting to read. It seems that these mice are really screwed up. Not only do they have a high susceptibility to EAE, but they also develop prolific cancers as well as spontaneous myopathy making it a model for muscular dystrophy. It does make one wonder if when this mouse is found to benefit from treatments for EAE, that it's actually also deriving some benefit for its other problems as well.
Quote:
SJL/J
Strain Former & Common Name(s): SJL; Swiss Jim Lambert
Important Note: This strain is homozygous for the retinal degeneration allele Pde6b rd1. Stock Number 000686
Application(s) Autoimmunity (experimental allergic encephalomyelitis (EAE))
Additional Research Areas
Cancer Research; Cardiovascular Research; Diabetes and Obesity Research; Mouse/Human Gene Homologs; Research Tools; Sensorineural Research
Phenotype SJL mice display a very high incidence of reticulum cell sarcomas resembling Hodgkin’s disease around one year of age. Sarcomas first appear in the Peyer’s patches and mesenteric lymph nodes and later in the spleen, liver, thymus and other lymph nodes. Most of the tumors are mixed-cell types classified as type B reticulum cell neoplasms, but a few are type A histiocytomas. This strain is also characterized by extreme aggression in males and its susceptibility to experimental autoimmune encephalomyelitis (EAE) for multiple sclerosis research. SJL/J mice develop a spontaneous myopathy resulting from a splice-site mutation in the Dysferlin gene. This Dysf im allele has been shown to result in decreased levels of dysferlin protein in SJL/J mice and makes this strain a good model for limb girdle muscular dystrophy 2B. This spontaneous myopathy is characterized by a progressive loss of muscle mass and strength corresponding with an increase in muscle pathology including muscle fibers with central nuclei, variation in size, splitting, inflammatory infiltrate, necrosis, and eventual replacement of muscle fiber with fat. While muscle weakness can be detected as early as three weeks of age the greatest pathology occurs after 6 months of age. SJL/J mice have also been shown to have an increased rate of muscle regeneration after injury when compared to BALB/c mice. SJL mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 000668, C57BR/cdJ, Stock No. 000667, and SM/J, Stock No. 000687). SJL/J are also useful as a control strain for studying immune defects in NOD/LtJ mice (Stock No. 001976), a model for type 1 diabetes (IDDM). Both NOD and SJL/J are derived from swiss mice; SJL are immunocompetent but have elevated levels of circulating T cells.
NHE