A bacterial effector protein promotes nuclear translocation of Stat3 to induce IL-10

Eur J Cell Biol. 2023 Oct 2;102(4):151364. doi: 10.1016/j.ejcb.2023.151364. Online ahead of print.ABSTRACTThe multifunctional Yersinia effector YopM inhibits effector triggered immunity and increases production of the anti-inflammatory cytokine Interleukin-10 (IL-10) to suppress the host immune response. Previously it was shown that YopM induces IL-10 gene expression by elevating phosphorylation of the serine-threonine kinase RSK1 in the nucleus of human macrophages. Using transcriptomics, we found that YopM strongly affects expression of genes belonging to the JAK-STAT signaling pathway. Further analysis revealed that YopM mediates nuclear translocation of the transcription factor Stat3 in Y. enterocolitica infected macrophages and that knockdown of Stat3 inhibited YopM-induced IL-10 gene expression. YopM-induced Stat3 translocation did not depend on autocrine IL-10, activation of RSK1 or tyrosine phosphorylation of Stat3. Thus, besides activation of RSK1, stimulation of nuclear translocation of Stat3 is another mechanism by which YopM increases IL-10 gene expression in macrophages.PMID:37806297 | DOI:10.1016/j.ejcb.2023.151364
Source: European Journal of Cell Biology - Category: Cytology Authors: Source Type: research