ArticleBlood2006
Critical role for Stat3 in T-dependent terminal differentiation of IgG B cells.
Article in Blood, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
79 citing papers in PubMed, 144 citations in OpenAlex.
- An IL-21R STAT hypomorph circumvents functional redundancy in germinal centre responses.eLife · 2026Article
- Building an Interleukin-10-Producing Identity: How B Cells Acquire Interleukin-10 Competence and How Plasma Cell Differentiation Consolidates This Program.Immunological reviews · 2026Review
- HDAC8 inhibition targets STAT3-MYC axis and synergizes with Venetoclax in KMT2A-rearranged acute myeloid leukemia.Leukemia · 2026Article
- STAT3 haploinsufficiency is associated with autosomal dominant hyper-IgE syndrome.Science advances · 2025Article
- Article
- STAT3 signaling in B cells controls germinal center zone organization and recycling.Cell reports · 2023Article
- Upregulated Expression of the IL-9 Receptor on TRAF3-Deficient B Lymphocytes Confers Ig Isotype Switching Responsiveness to IL-9 in the Presence of Antigen Receptor Engagement and IL-4.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- B cell-intrinsic STAT3-mediated support of latency and interferon suppression during murine gammaherpesvirus 68 infection revealed through anbioRxiv : the preprint server for biology · 2023Article
- The research development of STAT3 in hepatic ischemia-reperfusion injury.Frontiers in immunology · 2023Review
- Jmjd1c demethylates STAT3 to restrain plasma cell differentiation and rheumatoid arthritis.Nature immunology · 2022Article
- Harnessing the B Cell Response in Kidney Transplantation - Current State and Future Directions.Frontiers in immunology · 2022Review
- Germline STAT3 gain-of-function mutations in primary immunodeficiency: Impact on the cellular and clinical phenotype.Biomedical journal · 2021Review
- Evaluating the Role of STAT3 in CD4Infection and immunity · 2021Article
- IL-6 in inflammation, autoimmunity and cancer.International immunology · 2021Review
- Dual Role of Interleukin-10 in Murine NZB/W F1 Lupus.International journal of molecular sciences · 2021Article
- Expression Analysis of Protein Inhibitor of Activated STAT in Inflammatory Demyelinating Polyradiculoneuropathy.Frontiers in immunology · 2021Article
- Article
- STAT3 deficiency in B cells exacerbates uveitis by promoting expansion of pathogenic lymphocytes and suppressing regulatory B cells (Bregs) and Tregs.Scientific reports · 2020Article
- IL-21 is a broad negative regulator of IgE class switch recombination in mouse and human B cells.The Journal of experimental medicine · 2020Article
- Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 to Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution.Pharmacological reviews · 2020Review
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Stat proteins are latent cytoplasmic transcription factors that are crucial in many aspects of mammalian development. In the immune system, Stat3 has distinct roles in T-cell, neutrophil, and macrophage function, but a role for Stat3 in B-cell development, particularly in the terminal differentiation of B cells into antibody-secreting plasma cells, has never been directly tested. In this study, we used the Cre/lox system to generate a mouse strain in which Stat3 was conditionally deleted in the B-cell lineage (Stat3(fl/fl)CD19(Cre/+)). B-cell development, establishment of the peripheral B-cell compartment, and baseline serum antibody levels were unperturbed in Stat3(fl/fl)CD19(Cre/+) mice. Strikingly, Stat3(fl/fl)CD19(Cre/+) mice displayed profound defects in T-dependent (TD) IgG responses, but normal TD IgM, IgE, and IgA responses and T-independent (TI) IgM and IgG3 responses. In addition, germinal center (GC) formation, isotype switching, and generation of memory B cells, including IgG+ memory cells, were all intact in Stat3(fl/fl)CD19(Cre/+) mice, indicating that the requirement for Stat3 was limited to plasma cell differentiation. These results demonstrate a profound yet highly selective role for Stat3 in TD IgG plasma cell differentiation, and therefore represent a unique example of a transcription factor regulating isotype-specific terminal B-cell differentiation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.