IMMUNOLOGY2026™ Conference Recordings For Attendees-A BACH2-STAT5 transcriptional module licenses a short intracellular C3 proteoform in activated CD4+ T cells

A BACH2-STAT5 transcriptional module licenses a short intracellular C3 proteoform in activated CD4+ T cells

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Video Summary

Luis Trujillo presented work showing that the transcription factor BACH2 regulates CD4 T cell activation and helps prevent autoimmunity by controlling gene programs linked to STAT5 signaling. In BACH2 knockout CD4 T cells, RNA sequencing revealed increased IL-2/STAT5 and interferon pathways but decreased complement C3 expression. ChIP and enhancer-promoter analyses suggested BACH2 and STAT5 bind the C3 locus directly. Reporter mice, pharmacologic inhibition of IL-2/STAT5 signaling, and CRISPR targeting of bound regions all confirmed that both factors are required for C3 expression.  <br /><br />The study also found that activated CD4 T cells use an unusual internal C3 transcription start site, producing a short, likely intracellular C3 isoform that lacks a signal peptide. Its function is still unknown, but the work suggests BACH2 and STAT5 cooperate to shape a novel C3 proteoform in T cells.

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Date April 16, 2026 4:30 PM - 4:45 PM

Room 157

Session Molecular Mechanisms of T Cell Differentiation and Function

Speaker Jorge Trujillo

Track Immune Response Regulation: Molecular Mechanisms (IRM)

Year 2026

Keywords

BACH2

CD4 T cells

STAT5 signaling

complement C3

autoimmunity

April 16, 2026 4:30 PM - 4:45 PM

157

Molecular Mechanisms of T Cell Differentiation and Function

Jorge Trujillo

Immune Response Regulation: Molecular Mechanisms (IRM)

2026