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Regulation of CD40 function by its isoforms generated through alternative splicing.

M Tone1, Y Tone, P J Fairchild

  • 1Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, United Kingdom. mtone@molbiol.ox.ac.uk

Proceedings of the National Academy of Sciences of the United States of America
|February 15, 2001
PubMed
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Alternative splicing of CD40 mRNA creates isoforms that regulate immune cell signaling. Some CD40 variants block signaling, controlling cellular responses to CD40 ligand interactions.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Signaling

Background:

  • CD40 is a crucial receptor in the TNF receptor superfamily, mediating immune responses.
  • CD40-CD40L interaction activates key signaling pathways (NF-κB, JNK, JAK/STAT) essential for B cell function and cytokine production.

Purpose of the Study:

  • To investigate the role of alternative splicing in generating CD40 mRNA isoforms.
  • To determine how these isoforms are expressed in activated immune cells.
  • To assess the functional impact of CD40 isoforms on CD40-mediated signaling.

Main Methods:

  • Analysis of CD40 mRNA isoforms generated by alternative splicing.
  • Differential expression studies in activated macrophages and dendritic cells.
  • Reporter assays (IL-12 p40 gene expression) to evaluate CD40 signaling capacity.

Related Experiment Videos

Main Results:

  • Multiple CD40 mRNA isoforms arise from alternative splicing, with differential expression during immune cell activation.
  • Early activation favors signal-transducible CD40 mRNA; later stages show increased signal-non-transducible isoforms.
  • Three alternative isoforms were found to inhibit CD40 signaling, with a major isoform lacking the endodomain, potentially reducing cell surface functional CD40.

Conclusions:

  • CD40 expression is regulated post-transcriptionally and post-translationally via alternative splicing.
  • Alternative splicing of CD40 mRNA provides a mechanism for cells to control their responsiveness to CD40 ligand signaling.