ArticleThe Journal of experimental medicine2004
A B cell receptor with two Igalpha cytoplasmic domains supports development of mature but anergic B cells.
Article in The Journal of experimental medicine, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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Who cites it
8 citing papers in PubMed, 24 citations in OpenAlex.
- Review
- Role of inhibitory signaling in peripheral B cell tolerance.Immunological reviews · 2022Review
- Expression of the B-cell receptor component CD79a on immature myeloid cells contributes to their tumor promoting effects.PloS one · 2013Article
- Activation of the B cell receptor leads to increased membrane proximity of the Igα cytoplasmic domain.PloS one · 2013Article
- Homeostatic control of B lymphocyte subsets.Immunologic research · 2008Review
- Src-like adaptor protein (SLAP) regulates B cell receptor levels in a c-Cbl-dependent manner.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Essential role of membrane cholesterol in accelerated BCR internalization and uncoupling from NF-kappa B in B cell clonal anergy.The Journal of experimental medicine · 2006Article
- Ig beta tyrosine residues contribute to the control of B cell receptor signaling by regulating receptor internalization.The Journal of experimental medicine · 2006Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
Abstract
B cell receptor (BCR) signaling is mediated through immunoglobulin (Ig)alpha and Igbeta a membrane-bound heterodimer. Igalpha and Igbeta are redundant in their ability to support early B cell development, but their roles in mature B cells have not been defined. To examine the function of Igalpha-Igbeta in mature B cells in vivo we exchanged the cytoplasmic domain of Igalpha for the cytoplasmic domain of Igbeta by gene targeting (Igbetac-->alphac mice). Igbetac-->alphac B cells had lower levels of surface IgM and higher levels of BCR internalization than wild-type B cells. The mutant B cells were able to complete all stages of development and were long lived, but failed to differentiate into B1a cells. In addition, Igbetac-->alphac B cells showed decreased proliferative and Ca2+ responses to BCR stimulation in vitro, and were anergic to T-independent and -dependent antigens in vivo.
Indexed as
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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.