IMMUNOLOGY2026™ Conference Recordings For Attendees-HIPC Coordinating Center

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Video Summary

The speaker reviewed the CBM complex, especially CARD11, and its role in antigen receptor signaling in T and B cells. CARD11 mutations cause a range of “CARD11opathies”: complete deficiency leads to combined immunodeficiency, gain-of-function mutations cause BENTA disease with B-cell lymphoproliferation, and dominant-negative loss-of-function variants cause Caden’s disease, marked by severe atopy, high IgE, eosinophilia, and Th2 skewing. The lab uses reporter assays and patient cells to classify variants. Recent work showed that Caden’s disease is not explained by NF-kappaB defects alone: impaired JNK signaling may increase NFATC1 and GATA3, promoting Th2 responses. They also found the CBM complex controls expression of nutrient transporters ASCT2 and GLUT1, linking CARD11 to glutamine and glucose uptake and mTORC1 activation. These pathways influence T-cell differentiation. Potential treatments include dupilumab for Caden’s disease, sirolimus or B-cell depletion for some cases, and future strategies like glutamine supplementation and MALT1 inhibitors.

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Date April 18, 2026 8:00 AM - 9:30 AM

Room 153C

Session Systems-level Human Immune Profiling Data Resources and Analysis, Sponsored by the Human Immunol. Project Consortium (HIPC), La Jolla Inst. for Immunology

Speaker Bjoern Peters

Track Computational and Systems Immunology (COMP)

Year 2026

Keywords

CARD11

CBM complex

Caden's disease

BENTA disease

JNK signaling

mTORC1 activation

April 18, 2026 8:00 AM - 9:30 AM

153C

Systems-level Human Immune Profiling Data Resources and Analysis, Sponsored by the Human Immunol. Project Consortium (HIPC), La Jolla Inst. for Immunology

Bjoern Peters

Computational and Systems Immunology (COMP)

2026