IMMUNOLOGY2026™ Conference Recordings For Attendees-SLC7A5-mediated glutamine export is required for humoral immunity

Video Transcription

Video Summary

The talk presented research on <strong>SLC7A5/SLC3A2</strong>, an amino acid transporter that imports leucine and exports glutamine, in B-cell biology. The speaker found that this transporter is strongly induced during B-cell activation and in B-cell malignancy. Knocking it out caused selective defects: some malignant B-cell lines were impaired, but normal early B-cell development and maturation were largely unaffected. However, SLC7A5 was essential for <strong>germinal center responses</strong>, including <strong>class switch recombination, somatic hypermutation, plasma cell differentiation, and antibody affinity maturation</strong>.  

Mechanistically, the defects were not due to impaired B-cell receptor signaling. Instead, loss of SLC7A5 caused altered <strong>mTOR signaling</strong> and reduced <strong>AID expression</strong>. The key insight was that the critical function was likely <strong>glutamine export</strong>, not leucine uptake. Supporting this, an FDA-approved drug that provides an alternative glutamine export route partially rescued the class-switch defect. The work proposes glutamine export as a mechanism for <strong>ammonium detoxification</strong> important for humoral immunity.

Meta Tag

Date April 19, 2026 10:45 AM - 11:00 AM

Room 151

Session Regulation of B Cell Responses

Speaker Ruifeng Sun

Track Immune Response Regulation: Molecular Mechanisms (IRM)

Year 2026

Keywords

SLC7A5/SLC3A2

B-cell activation

germinal center responses

mTOR signaling

glutamine export

April 19, 2026 10:45 AM - 11:00 AM

151

Regulation of B Cell Responses

Ruifeng Sun

Immune Response Regulation: Molecular Mechanisms (IRM)

2026