The DOI matches its Crossref record; 17 of the 17 references it cites were found in a registry or an index.
Autoimmune disease in mice due to integration of an endogenous retrovirus in an apoptosis gene.
Open accessAbstract
The MRL-lpr/lpr mouse strain is a model of systemic autoimmune disease. In this model, intrinsic defects of intrathymic T cell development include defective deletion of self-reactive T cells and expression of endogenous retroviruses. Defective deletion of self-reactive T cells in the thymus has been proposed to be due to germline mutation in the Fas apoptosis gene. Using different fragments of a Fas cDNA probe, we determined that the lpr/lpr mutation is a 5.3-kb insertion of DNA within the second intron of the Fas gene. cDNA corresponding to this region was then derived from thymic RNA from MRL-lpr/lpr and MRL- +/+ mice using the polymerase chain reaction. All thymic RNA samples from MRL-lpr/lpr mice yielded a unique product that was 168 bp larger than that of MRL- +/+ mice. Complete sequence analysis indicated that this inserted sequence had 98% homology with a sequence from the 3' long terminal repeat of the early transposon (ETn). RNA analysis indicated higher expression of ETn RNA in the thymus of MRL-lpr/lpr than MRL- +/+ mice. The interdependence of ETn expression and abnormal Fas expression was then analyzed in a CD2-Fas transgenic mouse model in which a full-length murine Fas cDNA under the regulation of the CD2 promoter and enhancer was used to correct defective Fas expression in T cells of MRL-lpr/lpr mice. In these mice, reduced thymic ETn expression was observed, confirming that high ETn expression is related to abnormal Fas expression. These results establish a link between endogenous retrovirus expression, abnormal Fas expression, and autoimmune disease.
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Cites
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Cited by
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Metadata
- Authors
- Wu, J., Zhou, T., He, J., & Mountz, J. D.
- Venue
- The Journal of experimental medicine
- Publisher
- Rockefeller University Press
- Published
- 1993-08-01
- Volume
- 178
- Issue
- 2
- Pages
- 461-468
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2152508168
- Cited by
- 286
- References
- 17
- FWCI
- 14.86
- Type
- journal article
- Language
- en
- Open access
- green
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