Alternative splicing of the TNFSF13B (BAFF) pre-mRNA and expression of the 
BAFFX1 isoform in human immune cells

Stelmach, Patrick; Pütz, Michael; Pollmann, Robert; Happel, Michael; Stei, Susanne; Schlegel, Kerstin; Seipelt, Maria; Eienbroeker, Christian; Eming, Ruediger; Mandic, Robert; Huber, Magdalena; Tackenberg, Bjoern

doi:10.1016/j.gene.2020.145021

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Alternative splicing of the TNFSF13B (BAFF) pre-mRNA and expression of the BAFFX1 isoform in human immune cells

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Pütz, Michael
Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

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Citation

Stelmach, P., Pütz, M., Pollmann, R., Happel, M., Stei, S., Schlegel, K., et al. (2020). Alternative splicing of the TNFSF13B (BAFF) pre-mRNA and expression of the BAFFX1 isoform in human immune cells. GENE, 760: 145021. doi:10.1016/j.gene.2020.145021.

Cite as: https://hdl.handle.net/21.11116/0000-0008-BE3A-2

Abstract

Human B cell activating factor (TNFSF13B, BAFF) is a tumor necrosis
factor superfamily member. Binding its unique receptor (TNFRSF13C,
BAFF-R) mediates gene expression and cell survival in B cells via
activation of NF kappa B pathway. Furthermore, there is data indicating
a role in T cell function. A functionally inhibitory isoform (Delta
BAFF) resulting from the deletion of exon 3 in the TNFSF13B pre-RNA has
already been reported. However, data on the complexity of
post-transcriptional regulation is scarce. Here, we report molecular
cloning of nine TNFSF13B transcript variants resulting from alternative
splicing of the TNFSF13B pre-mRNA including BAFFX1. This variant is
characterized by a partial retention of intron 3 of the TNFSF13B gene
causing the appearance of a premature stop codon. We demonstrate the
expression of the corresponding BAFFX1 protein in Jurkat T cells, in ex
vivo human immune cells and in human tonsillar tissue. Thereby we
contribute to the understanding of TNFSF13B gene regulation and reveal
that BAFF is regulated through a post-transcriptional mechanism to a
greater extent than reported to date.