Trial reportThe Journal of clinical investigation2005
Unmutated and mutated chronic lymphocytic leukemias derive from self-reactive B cell precursors despite expressing different antibody reactivity.
Trial report in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers, 2 of them syntheses that pooled it.
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
150 citing papers in PubMed, 2 syntheses or guidelines pooled it, 330 citations in OpenAlex.
- Guideline
- Chronic lymphocytic leukemia and autoimmunity: a systematic review.Haematologica · 2011Pooled it
- Trial
- Trial
- Multiple productive immunoglobulin heavy chain gene rearrangements in chronic lymphocytic leukemia are mostly derived from independent clones.Haematologica · 2014Trial
- Stereotyped CLL-like immunoglobulin rearrangements in healthy repertoires: implications for leukemogenesis.Frontiers in immunology · 2026Review
- Defective cell-autonomous signalling and antigenic polyreactivity of B-cell receptors from chronic lymphocytic leukaemia stereotyped subset 1.Nature communications · 2025Article
- Chronic lymphocytic leukemia specificity analyses unveil bacterial lipopolysaccharides as the cognate ligands of established stereotyped BCR subsets.Blood cancer journal · 2025Article
- Insights into PI3K/AKT signaling in B cell development and chronic lymphocytic leukemia.FEBS letters · 2025Review
- SOX4 in chronic lymphocytic leukaemia: the forgotten transcription factor.Blood research · 2025Article
- Autoimmunity promotes chronic lymphocytic leukemia progression in an indolent disease model.Scientific reports · 2025Article
- JNK1 inhibitors target distal B cell receptor signaling and overcome BTK-inhibitor resistance in CLL.The Journal of experimental medicine · 2025Article
- Generation and Reactivity Profiling of Functional Human Recombinant Monoclonal Antibodies.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Conventional and non-conventional antigen-binding sites promote the development and function of chronic lymphocytic leukemia stereotyped subset #4 clones.Frontiers in immunology · 2025Article
- B Cell Differentiation and the Origin and Pathogenesis of Human B Cell Lymphomas.Methods in molecular biology (Clifton, N.J.) · 2025Review
- Expression Cloning of Antibodies from Single Human B Cells.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Article
- Characterization of antibody-dependent cellular phagocytosis in patients infected with hepatitis C virus with different clinical outcomes.Journal of medical virology · 2024Article
- The inhibitory receptor Siglec-G controls the severity of chronic lymphocytic leukemia.EMBO reports · 2023Article
- Review
90 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
8 authors at 3 institutions in 1 country.
Funding
Abstract
B cell chronic lymphocytic leukemia (CLL) is a disease of expanding monoclonal B cells whose B cell receptor (BCR) mutational status defines 2 subgroups; patients with mutated BCRs have a more favorable prognosis than those with unmutated BCRs. CLL B cells express a restricted BCR repertoire including antibodies with quasi-identical complementarity-determining region 3 (CDR3), which suggests specific antigen recognition. The antigens recognized by CLL antibodies may include autoantigens since about half of CLL B cells produce autoreactive antibodies. However, the distribution of autoreactive antibodies between Ig heavy-chain variable-unmutated (IgV-unmutated) CLL (UM-CLL) and IgV-mutated CLL (M-CLL) is unknown. To determine the role of antibody reactivity and the impact of somatic hypermutation (SHM) on CLL antibody specificity, we cloned and expressed in vitro recombinant antibodies from M- and UM-CLL B cells and tested their reactivity by ELISA. We found that UM-CLL B cells expressed highly polyreactive antibodies whereas most M-CLL B cells did not. When mutated nonautoreactive CLL antibody sequences were reverted in vitro to their germline counterparts, they encoded polyreactive and autoreactive antibodies. We concluded that both UM-CLLs and M-CLLs originate from self-reactive B cell precursors and that SHM plays an important role in the development of the disease by altering original BCR autoreactivity.
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.