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Title

An MRL/MpJ-lpr/lpr substrain with a limited expansion of lpr double-negative T cells and a reduced autoimmune syndrome

Authors
Fossati-Jimack, Liliane
Takahashi, Satoru
Merino, Ramon
Iwamoto, Masahiro
Aubry, J. P.
Nose, M.
Spach, C.
Motta, R.
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Published in International Immunology. 1993, vol. 5, no. 5, p. 525-532
Abstract The autosomal recessive mutant gene, lpr, has been shown to accelerate the progression of lupus-like autoimmune disease, which is associated with a massive expansion of a unique CD4-CD8- double-negative T cell subset, in MRL/MpJ mice. Here we report a substrain of MRL/MpJ-lpr/lpr (MRL-lpr) mice which live almost twice as long with delayed development of glomerulonephritis, compared with conventional MRL-lpr mice. This substrain, termed MRL-lpr.II (II for long-lived), develops generalized lymphadenopathy characteristically seen in MRL-lpr mice. However, the expansion of a double negative lpr T cell subset is markedly limited with a mean value of 15% in their lymph nodes compared to about 70% in conventional MRL-lpr mice. Overall production of autoantibodies, such as anti-DNA and rheumatoid factors, does not significantly differ between the two MRL-lpr mice. However, serum levels of cryoglobulins, whose major component is IgG3, are markedly diminished in MRL-lpr.II mice with a parallel decrease in IgG3. Since MRL-lpr.II mice still carry the lpr mutation, as documented by the presence of defects in the Fas antigen, a possible new mutation in this substrain may play a significant role in the pathogenesis of lupus-like autoimmune syndrome.
Keywords AnimalsAutoantibodies/biosynthesisAutoimmune Diseases/ geneticsCryoglobulins/biosynthesisFemaleGenes, RecessiveGlomerulonephritis/genetics/immunology/pathologyLongevity/geneticsLymphocyte ActivationMaleMiceMice, Mutant Strains/ genetics/ immunologySpecies SpecificitySyndromeT-Lymphocyte Subsets/ immunology
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PMID: 8318455
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