| Autor: |
Koch-Nolte, Friedrich, Klein, Johannes, Hollmann, Christiane, Kühl, Maren, Haag, Friedrich, Gaskins, H. Rex, Leiter, Edward, Thiele, Heinz-Günter |
| Zdroj: |
International Immunology; May1995, Vol. 7 Issue 5, p883-890, 8p |
| Abstrakt: |
Rt6 is a T cell-restricted GPI-anchored membrane protein and a member of the family of mono(ADP-ribosyl)transferases. One of the two murine genes is deleted in NZW mice. This finding is reminiscent of the deletion of one of the β genes in the same mouse strain and it is an intriguing possibility that these gene deletions arose by a common genetic mechanism. The locus retained by the NZW mouse (designated -1) is polymorphic among inbred strains of laboratory mice. The NZW mouse shows several strain-specific restriction fragment length variants in this locus and five amino acid substitutions occur in the predicted native polypeptide of the NZW mouse relative to the corresponding polypeptides of NZB and BALB/c mice. Whereas transcript levels of the two genes appear to be normal in spleen and intestine of NZB mice, the corresponding tissues of NZW mice show reduced levels of transcripts from the locus retainedin this mouse strain. Moreover, reduced levels of mRNA also occur in spleen and intestine of (NZB × NZW)F hybrid animals, indicating that F animals have inherited a dominant factor from the genetic background of the NZW mouse, resulting in low levels of expression. It is conceivable that the alterations in the genes of the NZW mouse and/or the factor(s) affecting defective expression constitute part of the genetic contribution of the NZW mouse to the autoimmune lupus-like disease in (NZB × NZW)F animals. Interestingly, a deficiency of -expressing cells evidenced by reduced mRNA levels has previously also been observed in association with autoimmune disease in the BB-DP rat and NOD mouse animal models for autoimmune diabetes mellitus. The results presented here provide support for the hypotheses that a subset of regulatory T cells confers protection to autoimmune disease in different animal models and that failure to develop this subset can result in enhanced susceptibility for autoimmune disease. [ABSTRACT FROM PUBLISHER] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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