ArticleImmunology2003
A differential requirement for phosphoinositide 3-kinase reveals two pathways for inducible upregulation of major histocompatibility complex class II molecules and CD86 expression by murine B lymphocytes.
Article in Immunology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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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
7 citing papers in PubMed, 18 citations in OpenAlex.
- Pomalidomide restores immune recognition of primary effusion lymphoma through upregulation of ICAM-1 and B7-2.PLoS pathogens · 2021Article
- Deep Phenotyping of CD11cFrontiers in immunology · 2021Article
- CTLA-4 controls follicular helper T-cell differentiation by regulating the strength of CD28 engagement.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- B cells regulate CD4+ T cell responses to papain following B cell receptor-independent papain uptake.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- IL-21 promotes CD4 T cell responses by phosphatidylinositol 3-kinase-dependent upregulation of CD86 on B cells.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Article
- Single round of antigen receptor signaling programs naive B cells to receive T cell help.Immunity · 2010Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Constitutive expression of major histocompatibility complex class II molecules (MHC II) is restricted to dendritic cells, cells of the macrophage lineage and B lymphocytes. In all three lineages, peptide fragments of captured antigen are loaded into newly synthesized MHC II molecules. In B-lineage cells, MHC II synthesis is dramatically increased on encounter with antigen, by T-cell-derived signals and by microbial products. We have previously shown that immature B cells fail to hyperexpress MHC II after antigen receptor [B-cell receptor (BCR)] ligation, but are responsive to other stimuli. Expression of the costimulatory molecule, CD86, was similarly regulated. This suggested the existence of two pathways regulating expression of these important molecules. Here we present data supporting this hypothesis. We show that activity of the enzyme phosphatidylinositol 3-kinase is critical for MHC II hyperexpression and induction of CD86 in response to ligation of the BCR or CD38, but not for responses to other stimuli including interleukin-4, lipopolysaccharide and CD40 ligation.
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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.