ArticleNature immunology2009
CD98hc facilitates B cell proliferation and adaptive humoral immunity.
Article in Nature immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
What it found
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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.
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
68 citing papers in PubMed, 118 citations in OpenAlex.
- Infection-induced plasmablasts are a nutrient sink that impairs humoral immunity to malaria.Nature immunology · 2020Trial
- Constructing cell-type-specific gene regulatory networks from cell-cell communication and a global gene regulatory network.Briefings in bioinformatics · 2026Article
- Proteolysis at the extracellular matrix interface: Molecular architects and regulators in health and disease.The FEBS journal · 2026Review
- Lipopolysaccharide stimulates dynamic changes in B cell metabolism to promote proliferation.eLife · 2026Article
- SLC7A5 regulates B cell metabolism and plasma cell differentiation independent of leucine transport.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Schistosome esophageal gland factor MEG-8.2 drives host cell lysis and interacts with host immune proteins.PLoS pathogens · 2026Article
- Novel immunotargets in multiple myeloma: biological relevance and therapeutic potential.Biomarker research · 2025Review
- Loss of CD98HC phosphorylation by ATM impairs antiporter trafficking and drives glutamate toxicity in Ataxia telangiectasia.Nature communications · 2025Article
- Screening the human miRNA interactome reveals coordinated up-regulation in melanoma, adding bidirectional regulation to miRNA networks.Science advances · 2025Article
- Leveraging a disulfidptosis-based signature to characterize heterogeneity and optimize treatment in multiple myeloma.Frontiers in immunology · 2025Article
- Asparagine availability controls germinal center B cell homeostasis.Science immunology · 2024Article
- Lipid metabolism in B cell biology.Molecular oncology · 2024Review
- Advances in nanomaterial-targeted treatment of acute lung injury after burns.Journal of nanobiotechnology · 2024Review
- Harnessing Immune Cell Metabolism to Modulate Alloresponse in Transplantation.Transplant international : official journal of the European Society for Organ Transplantation · 2024Review
- Glutaminolysis of CD4Journal of inflammation research · 2024Review
- Review
- Integrin β1 regulates marginal zone B cell differentiation and PI3K signaling.The Journal of experimental medicine · 2023Article
- CD98 heavy chain as a prognostic biomarker and target for cancer treatment.Frontiers in oncology · 2023Review
- CD98hc as a marker of radiotherapy-resistant cancer stem cells in head and neck squamous cell carcinoma.Archives of medical science : AMS · 2023Article
- Identification of CD98 as a Novel Biomarker for HIV-1 Permissiveness and Latent Infection.mBio · 2022Article
8 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
7 authors at 4 institutions in 3 countries.
Funding
Abstract
The proliferation of antigen-specific lymphocytes and resulting clonal expansion are essential for adaptive immunity. We report here that B cell-specific deletion of the heavy chain of CD98 (CD98hc) resulted in lower antibody responses due to total suppression of B cell proliferation and subsequent plasma cell formation. Deletion of CD98hc did not impair early B cell activation but did inhibit later activation of the mitogen-activated protein kinase Erk1/2 and downregulation of the cell cycle inhibitor p27. Reconstitution of CD98hc-deficient B cells with CD98hc mutants showed that the integrin-binding domain of CD98hc was required for B cell proliferation but that the amino acid-transport function of CD98hc was dispensable for this. Thus, CD98hc supports integrin-dependent rapid proliferation of B cells. We propose that the advantage of adaptive immunity favored the appearance of CD98hc in vertebrates.
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.