ArticleJournal of immunology (Baltimore, Md. : 1950)2009
Activation-induced cytidine deaminase expression and activity in the absence of germinal centers: insights into hyper-IgM syndrome.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 50 citations in OpenAlex.
- The mechanisms of human lymphoid chromosomal translocations and their medical relevance.Critical reviews in biochemistry and molecular biology · 2022Article
- Diversity upon diversity: linking DNA double-strand break repair to blood cancer health disparities.Trends in cancer · 2022Review
- Primary germinal center-resident T follicular helper cells are a physiologically distinct subset of CXCR5Immunity · 2022Article
- The role of B cells in COVID-19 infection and vaccination.Frontiers in immunology · 2022Review
- Activation induced cytidine deaminase: An old friend with new faces.Frontiers in immunology · 2022Review
- Mechanistic basis for chromosomal translocations at the E2A gene and its broader relevance to human B cell malignancies.Cell reports · 2021Article
- An Unmutated IgM Response to the Vi Polysaccharide ofJournal of immunology (Baltimore, Md. : 1950) · 2018Article
- Chronic Lymphocytic Leukemia B-Cell Normal Cellular Counterpart: Clues From a Functional Perspective.Frontiers in immunology · 2018Review
- BCR and Endosomal TLR Signals Synergize to Increase AID Expression and Establish Central B Cell Tolerance.Cell reports · 2017Article
- Host controls of HIV broadly neutralizing antibody development.Immunological reviews · 2017Review
- Efficient Culture of Human Naive and Memory B Cells for Use as APCs.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Mechanisms of human lymphoid chromosomal translocations.Nature reviews. Cancer · 2016Review
- Article
- Activation-Induced Cytidine Deaminase Expression in Human B Cell Precursors Is Essential for Central B Cell Tolerance.Immunity · 2015Article
- Article
- Metabolic reprogramming is required for antibody production that is suppressed in anergic but exaggerated in chronically BAFF-exposed B cells.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Primary cold agglutinin-associated lymphoproliferative disease: a B-cell lymphoma of the bone marrow distinct from lymphoplasmacytic lymphoma.Haematologica · 2014Article
- Flexible ordering of antibody class switch and V(D)J joining during B-cell ontogeny.Genes & development · 2013Article
- The human fetal lymphocyte lineage: identification by CD27 and LIN28B expression in B cell progenitors.Journal of leukocyte biology · 2013Article
- Targeting antigens to CD180 rapidly induces antigen-specific IgG, affinity maturation, and immunological memory.The Journal of experimental medicine · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Somatic hypermutation normally occurs as a consequence of the expression of activation-induced cytidine deaminase (AID) by Ag-activated, mature B cells during T cell-dependent germinal center responses. Nonetheless, despite their inability to express CD154 and initiate GC responses, patients with type 1 hyper-IgM syndrome (HIGM1) support populations of IgM(+)IgD(+)CD27(+) B cells that express mutated Ig genes. The origin of these mutated B cells is unknown; the IgM(+)IgD(+)CD27(+) cells do not express AID and appear to acquire mutations independent of stringent selection by Ag. Here, we demonstrate that immature/transitional 1 B cells from the bone marrow of CD154-deficient mice express AID and acquire Ig mutations that lack the hallmarks of antigenic selection via BCR signaling. Comparable levels of AID expression was found in developmentally immature B cells recovered from murine fetal liver and from human immature/transitional 1 B cells recovered from umbilical cord blood. AID expression in human fetal liver was also robust, approaching that of human tonsil tissue and the human germinal center B cell line, Ramos. These observations led us to conclude that AID expression in developing human B cells is the origin of the mutated IgM(+)IgD(+)CD27(+) B cells present in HIGM1 patients, and we propose that both mice and humans share a latent, AID-dependent pathway for the preimmune diversification of B lymphocytes that is more prominent in chicken, sheep, and rabbits.
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.