STAT3
Overview
STAT3 is the transcription factor downstream of the IL-21R and the wiki’s only measured JAK-STAT readout. It matters here because phospho-STAT3 is the assay that demonstrates IFN-γ priming works — it is the point at which “IFN-γ reprograms the cell” stops being an inference from chromatin and becomes a measured signalling difference.
⚠ Thin page — single source. Every claim below traces to Zumaquero2019 - IFN-gamma Programs T-bet-hi B Cells for ASC Differentiation. The wiki has no page for STAT1 or STAT5, and no JAK content at all, because no ingested source supplies more than a motif-level or predicted mention. Treat this page as a stub pending a second source.
Key Points from Literature
- Basal phospho-STAT3 at day 3 was similar and low across all culture conditions (no cytokine, IL-2, IFN-γ, or IFN-γ+IL-2), with only a modest elevation in the combined condition (see Zumaquero2019 - IFN-gamma Programs T-bet-hi B Cells for ASC Differentiation, human in vitro, ≥3 experiments)
- After 20 minutes of IL-21 exposure, phospho-STAT3 was significantly increased in B cells that had been exposed to IFN-γ during the priming phase — the functional demonstration that early IFN-γ enhances IL-21R signalling (see Zumaquero2019 - IFN-gamma Programs T-bet-hi B Cells for ASC Differentiation)
- STAT3 and STAT1 were both predicted upstream regulators of the T-bet^hi^ DN2 pre-ASC transcriptional network by Ingenuity Pathway Analysis, alongside BTK, IFNα, IFN-γ, IL-2 and IL-21 (see Zumaquero2019 - IFN-gamma Programs T-bet-hi B Cells for ASC Differentiation, human RNA-seq — a prediction, not a measurement)
- Related but distinct: STAT5 binding motifs showed enriched chromatin accessibility in IL-2-exposed B cells, and the greatest enrichment when IFN-γ was also present (see Zumaquero2019 - IFN-gamma Programs T-bet-hi B Cells for ASC Differentiation, ATAC-seq n=2–3/group). STAT5 has no page.
- Background context (not from an ingested source): in mouse SLE models, clinical disease is dependent on B-cell-specific expression of the IFN-γ receptor and STAT1 — cited in Zumaquero2019 - IFN-gamma Programs T-bet-hi B Cells for ASC Differentiation’s introduction from un-ingested work.
Contradictions & Debates
None recorded — the page has only one source. The absence of contradictions here reflects lack of coverage, not consensus.
Related Pages
IL-21R, IL-21, IFN-gamma, B Cell Receptor Signaling, Extrafollicular T Cell Help, Phospho-Flow Cytometry, DN2 B Cell