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Accumulation of splice variants and transcripts in response to PI3K inhibition in T cells

Alice Riedel1, Boitumelo Mofolo, Elita Avota

  • 1Institute for Virology and Immunobiology, University of Wuerzburg, Versbacher, Wuerzburg, Germany.

Plos One
|February 6, 2013
PubMed
Abstract

Insights

Measles virus impairs T cell function by altering gene expression and alternative splicing, leading to T cell suppression. These changes impact key pathways for T cell activation and signaling.

Area of Science:

  • Immunology
  • Molecular Biology
  • Virology

Background:

  • Measles virus (MV) induces T cell suppression by interfering with phosphatidylinositol-3-kinase (PI3K) activation.
  • This interference affects splice regulatory proteins, leading to the production of inhibitory protein isoforms via alternative splicing.

Purpose of the Study:

  • To investigate how PI3K abrogation in T cells leads to differentially regulated and alternatively spliced transcripts.
  • To determine if these variant transcripts encode proteins involved in T cell silencing.

Main Methods:

  • Human Exon 1.0 ST Array performed on T cells with and without PI3K inhibition.
  • Development of a splicing index algorithm to identify alternative splicing (AS) and differential gene regulation (RG).

Main Results:

  • 9% of genes showed alternative splicing (AS), while 3% exhibited differential regulation (RG).
  • AS genes were enriched in extracellular matrix (ECM)-receptor interaction and focal adhesion pathways.
  • RG genes were enriched in cytokine-receptor interaction and Jak-STAT pathways.
  • Combined AS/RG alterations affected T cell receptor signaling, cytoskeletal dynamics, and cell cycle entry.

Conclusions:

  • PI3K abrogation disrupts T cell activation through both differential expression and alternative splicing.
  • These molecular changes collectively contribute to measles virus-induced T cell suppression.

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