TACI
Overview
TACI (TNFRSF13B) binds both BAFF and APRIL. In this wiki it appears in two distinct roles: as a blocking reagent (TACI-Fc, a decoy receptor used to neutralise both ligands) and as a surface receptor on atypical B cells whose expression sits oddly against those cells’ reported BAFF-independence.
Key Points from Literature
- ★ TACI-Fc blockade reduced B cell proliferation and plasmablast differentiation in a dengue monocyte–B cell coculture, and significantly reduced IgM production (see Kwissa2014 - Monocytes Drive Plasmablast Differentiation in Dengue, human in vitro, 4 donors). TACI-Fc neutralises both BAFF and APRIL, so this establishes the axis but not which ligand.
- ABCs express BAFF-R and TACI and can consume or sequester BAFF, yet are themselves largely BAFF-independent — proposed to make them exceptional competitors in BAFF-regulated homeostatic space (see Cancro2020 - Age-Associated B Cells, review, murine, zero original data — sole source)
- BCMA (Tnfrsf17), the third receptor for BAFF and APRIL, was among the most highly expressed genes in murine T-bet⁺CD11c⁺ B cells (see Song2022 - Tfh Outside Germinal Centers Drive T-bet CD11c B Cells, murine RNA-seq). Covered on BAFF.
Contradictions & Debates
Why express a receptor you do not depend on? Cancro2020 - Age-Associated B Cells’s account has ABCs expressing TACI and BAFF-R while being functionally BAFF-independent, using the receptors to sequester ligand rather than to receive a survival signal. This is an elegant hypothesis but rests on a single murine review with no original data, and no ingested source has tested ligand consumption directly. Meanwhile TACI-Fc blockade does reduce plasmablast output in a human dengue system, which is at least consistent with the receptors being functional. Recorded as open — see the full three-way tension on BAFF.
Related Pages
BAFF, APRIL, Age-Associated B Cell, Plasmablast, Inflammatory Monocyte, Atypical B Cell Effector Output