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CD82 regulates STAT5/IL‐10 and supports survival of acute myelogenous leukemia cells

We recently reported that adhesion molecule CD82 is aberrantly expressed in CD34+/CD38− leukemia stem cells (LSCs). Here, we report the results of a functional analysis of CD82 in CD34+/CD38− acute myelogenous leukemia (AML) cells. Short hairpin (sh)RNA‐mediated downregulation of CD82 resulted in a decrease in the level of IL‐10. In contrast, forced expression of CD82 in CD34+/CD38+ AML cells by transduction with CD82‐expressing lentiviral particles resulted in an increase in the levels of IL‐10. Notably, exposure of CD34+/CD38− AML cells to IL‐10 stimulated clonogenic growth of these cells. Moreover, downregulation of CD82 by a shRNA dephosphorylated STAT5 in CD34+/CD38− AML cells. On the other hand, forced expression of CD82 resulted in increase in the levels of p‐STAT5 in CD34+/CD38+ AML cells. Chromatin immunoprecipitation (ChIP) assay results indicated that STAT5A binds to the promoter region of the IL‐10 gene, while reporter gene assay results indicated stimulation of IL‐10 expression at the transcriptional level. These results suggest that CD82 positively regulates the STAT5/IL‐10 signaling pathway. Moreover, shRNA‐mediated downregulation of CD82 expression in CD34+/CD38‐ AML cells dephosphorylated STAT5 in immunodeficient mice. Taken together, our data suggest that the CD82/STAT5/IL‐10 signaling pathway is involved in the survival of CD34+/CD38− AML cells and may thus be a promising therapeutic target for eradication of AML LSCs.