APRIL
Overview
APRIL (TNFSF13) is the close relative of BAFF, sharing the receptors TACI and BCMA but not BAFF-R. In this wiki APRIL is almost always measured and blocked together with BAFF, so its independent contribution is rarely separable. The main page for the axis and its unresolved contradiction is BAFF.
Key Points from Literature
- Genes encoding BAFF and APRIL were increased in the blood of dengue patients with high viraemia at the early stage, and correlated with the magnitude of the CD14⁺CD16⁺ monocyte population (see Kwissa2014 - Monocytes Drive Plasmablast Differentiation in Dengue, n=28 acute secondary dengue)
- APRIL protein trended higher in the plasma of high-viral-load patients, and DENV-infected monocytes secreted APRIL in vitro (see Kwissa2014 - Monocytes Drive Plasmablast Differentiation in Dengue)
- TACI-Fc — which blocks both APRIL and BAFF — modestly diminished B cell proliferation and plasmablast differentiation, and significantly reduced IgM production (see Kwissa2014 - Monocytes Drive Plasmablast Differentiation in Dengue, human in vitro, 4 donors). Because TACI-Fc is not APRIL-selective, this does not isolate APRIL’s contribution.
- BLyS and APRIL support CD40-independent class switch recombination (see Wei2007 - DN Memory B Cells in SLE, citing Litinskiy 2002 — not ingested). This is potentially significant for the extrafollicular pathway, where CD40L is reported to inhibit differentiation (see Jenks2018 - DN2 B Cells and EF Pathway in SLE) — a CD40-independent route to class switching would be required. See Class Switch Recombination.
- Serum APRIL, measured alongside BAFF, IL-6, IL-10 and IL-21, showed no correlation with plasmablast magnitude in dengue (see GarciaBates2013 - Plasmablast Response and Dengue Severity, dengue primary)
Contradictions & Debates
The APRIL evidence is subsumed in the three-way BAFF/APRIL tension documented on BAFF — transcript correlation and functional blockade in one dengue primary versus a serum-protein null in another. Not repeated here.
A gap worth naming: the CD40-independent CSR route attributed to BLyS/APRIL is potentially the mechanism that reconciles class switching in the extrafollicular pathway with CD40L’s inhibitory effect on EF differentiation. No ingested source tests this. The supporting citation (Litinskiy 2002) is not in the wiki.
Related Pages
BAFF, TACI, Class Switch Recombination, CD40L, Plasmablast, Inflammatory Monocyte, Extrafollicular Response