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. 2019 May 29;14(5):e0216898. doi: 10.1371/journal.pone.0216898

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© 2019 Nagel et al

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Fig 5 — This diagram combines the results of our study with data from the literature as indicated in the text. EBV activates IRF4 and STAT3 which in turn activates expression of NKL homeobox gene HLX. HLX is located in a central position of this network. Downstream targets of HLX are NKL homeobox genes MSX1 and NKX6-3, plasma cell factors IL4R and SPIB, and pro-apoptotic factor BCL2L11. Our data indicate that HLX inhibits plasma cell differentiation via NKX6-3, IL4R and SPIB and apoptosis via BCL2L11. Developmental regulators BCL6, BACH2, PRDM1 and IRF4 regulate each other and are targeted directly or indirectly by EBV. Upregulated genes/modifications in EBV-positive DOHH-2 cells are indicated in red, downregulated genes/modifications in green and genes showing no alterations in expression levels in black. NKL homeobox genes are boxed in grey.