[HTML][HTML] An autoimmune disease prevented by anti-retroviral drugs
GB Beck-Engeser, D Eilat, M Wabl - Retrovirology, 2011 - Springer
GB Beck-Engeser, D Eilat, M Wabl
Retrovirology, 2011•SpringerAbstract Background Both Aicardi-Goutières syndrome, a Mendelian mimic of congenital
infection, and the autoimmune disease systemic lupus erythematosus can result from
mutations in the gene encoding the enzyme Trex1. In mice, the absence of Trex1 causes
severe myocarditis. The enzyme is thought to degrade endogenous retroelements, thus
linking them to autoimmune disease. However, inhibition of reverse transcription by the
inhibitor zidovudine (AZT) did not ameliorate the disease, weakening the link to …
infection, and the autoimmune disease systemic lupus erythematosus can result from
mutations in the gene encoding the enzyme Trex1. In mice, the absence of Trex1 causes
severe myocarditis. The enzyme is thought to degrade endogenous retroelements, thus
linking them to autoimmune disease. However, inhibition of reverse transcription by the
inhibitor zidovudine (AZT) did not ameliorate the disease, weakening the link to …
Background
Both Aicardi-Goutières syndrome, a Mendelian mimic of congenital infection, and the autoimmune disease systemic lupus erythematosus can result from mutations in the gene encoding the enzyme Trex1. In mice, the absence of Trex1 causes severe myocarditis. The enzyme is thought to degrade endogenous retroelements, thus linking them to autoimmune disease. However, inhibition of reverse transcription by the inhibitor zidovudine (AZT) did not ameliorate the disease, weakening the link to retroelements.
Findings
Here, we show that two other FDA-approved drugs that inhibit reverse transcriptase can ameliorate the myocarditis in Trex1-null mouse.
Conclusions
The result suggests that retroelements contribute to this hereditary form of autoimmunity, and that treatment with retroelement inhibitors might ameliorate Aicardi-Goutières syndrome in humans.
Springer