| Autor: |
Fossati, Liliane, Takahashi, Satoru, Merino, Ramón, Iwamoto, Masahiro, Aubry, Jean-Pierre, Nose, Masato, Spach, Colette, Motta, Roland, Izui, Shozo |
| Zdroj: |
International Immunology; May1993, Vol. 5 Issue 5, p525-532, 8p |
| Abstrakt: |
The autosomal recessive mutant gene, , has been shown to accelerate the progression of lupus-like autoimmune disease, which is associated with a massive expansion of a unique CD4CD8 double-negative T cell subset, in MRL/MpJ mice. Here we report a substrain of MRL/MpJ- (MRL-) mice which live almost twice as long with delayed development of glomerulonephritis, compared with conventional MRL- mice. This substrain, termed MRL- ( for long-lived), develops generalized lymphadenopathy characteristically seen in MRL- mice. However, the expansion of a double negative T cell subset is markedly limited with a mean value of 15% in their lymph nodes compared to about 70% in conventional MRL- mice. Overall production of autoantibodies, such as anti-DNA and rheumatoid factors, does not significantly differ between the two MRL- mice. However, serum levels of cryoglobulins, whose major component is lgG3, are markedly diminished in MRL- mice with a parallel decrease in lgG3. Since MRL- mice still carry the 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 pathogenesls of lupus-like autoimmune syndrome. [ABSTRACT FROM PUBLISHER] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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