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Manipulating CD38 ectoenzymatic activity revitalizes regulatory T cells via deacetylase Sirt-1 in immune thrombocytopenia
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DOI：10.1016/j.jtha.2026.06.019.png)
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Abstract
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Immune thrombocytopenia (ITP) is the most common acquired bleeding disorder where considerable dysfunction of regulatory T cells (Tregs) contributes to the loss of immune tolerance. CD38 is a transmembrane glycoprotein equipped with ectoenzymatic activities. It affects other NAD+-consuming enzymes such as deacetylase Sirtuin-1 (Sirt-1), which is pivotal for Treg stability. Anti-CD38 monoclonal antibodies exert ectoenzyme-modulating capacity and has been proven to rapidly boost and maintain platelet levels in patients with ITP.
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