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Beta hemoglobinopathies are widely spread monogenic lethal diseases.  Delta-globin  gene activation has been proposed as a possible approach for curing these pathologies. The therapeutic potential of delta-globin, the non-alpha component of Hemoglobin A 2  (α2δ2; HbA2), has been demonstrated in a mouse model of beta thalassemia, while its anti-sickling effect, comparable to that of gamma globin, was established some time ago. Here we show that the  delta-globin  mRNA level is considerably increased in a  Deoxyribonuclease II-alpha  knockout mouse model in which type 1 interferon (interferon beta, IFNb) is activated. IFNb activation in the fetal liver improves the  delta-globin  mRNA level, while the  beta-globin  mRNA level is significantly reduced. In addition, we show that HbA2 is significantly increased in patients with multiple sclerosis under type 1 interferon treatment. Our results represent a proof of principle that delta-globin expression can be enhanced through the use of molecules. This observation is potentially interesting in view of a pharmacological approach able to increase the HbA2 level.

Delta-Globin Gene Expression Is Enhanced in vivo by Interferon Type I