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"Natural" RT6-1 and RT6-2 "knock-out" mice
M Matthes1, C Hollmann, H Bertuleit
1Department of Immunology, University Hospital, Hamburg, Germany.
Advances in Experimental Medicine and Biology
|January 1, 1997
Summary
Certain mouse strains exhibit natural gene defects in Rt6-2 or Rt6-1, acting as single-gene knockouts. These genetic variations are investigated for their role in autoimmune diseases like lupus.
Area of Science:
- Immunology
- Genetics
- Mouse Models of Disease
Background:
- The Rt6 gene family plays a role in immune regulation.
- Mouse strains with susceptibility to autoimmune diseases were examined for Rt6 gene expression.
- Deviations in Rt6 gene expression can indicate underlying genetic abnormalities.
Purpose of the Study:
- To screen various mouse strains for alterations in Rt6 gene expression.
- To identify natural 'knockout' models for Rt6-1 and Rt6-2 genes.
- To investigate the association between Rt6 gene defects and autoimmune diseases.
Main Methods:
- RT-PCR was used to screen for Rt6 gene expression across different mouse strains.
- Southern blot and sequence analyses were performed to confirm gene deletions or mutations.
- Immunological assessments were conducted on affected mouse strains.
Main Results:
- NZW mice lack detectable Rt6-2 gene transcripts due to a gene deletion.
- BxSB mice exhibit a near-complete absence of Rt6-1 gene transcripts due to a premature stop codon.
- NZW mice show no gross immunological abnormalities, suggesting Rt6-2 loss alone has no obvious phenotype.
Conclusions:
- NZW and BxSB mice serve as natural models for Rt6-2 and Rt6-1 single-gene knockouts, respectively.
- Spontaneous Rt6 gene defects may contribute to the polygenetic basis of autoimmune diseases in these strains.
- Further research is needed to elucidate the role of these Rt6 gene defects in systemic autoimmune diseases.

