The long noncoding RNA (lncRNA) growth arrest specific 5 (GAS5) can regulate the balance of T helper 17 (Th17)/regulatory T (Treg) cells in myasthenia gravis by targeting miR-23a expression, according to a new study published in the Journal of International Medical Research.
This finding provides a scientific basis for the development of clinical therapeutics for the disease, according to the authors.
Recently, lncRNAs have attracted the attention of researchers due to the role they play in the pathogenesis of many diseases.
In the present study, researchers from China analyzed the levels of GAS5 and miR-23a expression as well as the proportion of Th17 and Treg cells in CD4+ T cells obtained from patients with myasthenia gravis.
Read more about the pathophysiology of myasthenia gravis.
They found that the levels of GAS5 were significantly decreased in patient cells. They also showed that the overexpression of GAS5 inhibited the differentiation of Th17 in CD4+ T cells.
The researchers confirmed that miR-23a is a downstream target of GAS5 and that GAS5 negatively regulates miR-23a through direct interaction.
Finally, they showed that GAS5 can inhibit the differentiation of Th17 by downregulating miR-23a.
“Our study illustrates that GAS5 expression is decreased in [myathenia gravis] and can inhibit Th17 differentiation by directly targeting miR-23a,” the authors concluded. “These findings may provide novel insights into the pathogenesis of this disease.”
Myasthenia gravis is a rare autoimmune disease but the most common disease affecting the neuromuscular junction. It is characterized by an immune attack against acetylcholine receptors on the postsynaptic motor membrane inhibiting the transition of normal nerve signals to the muscles.
The exact cause of the disease is not known and in most cases the development of autoimmunity is idiopathic. In some cases, the disease may be triggered by viral or bacterial infections.
Xu Y, Ouyang Y. Long non-coding RNA growth arrest specific 5 regulates the T helper 17/regulatory T balance by targeting miR-23a in myasthenia gravis. J Int Med Res. 2022;50(6):3000605211053703. doi:10.1177/03000605211053703