ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Loss of T cell CD98 H chain specifically ablates T cell clonal expansion and protects from autoimmunity.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 84 citations in OpenAlex.
- Boosting CAR T cell efficacy in cancer with metabolic insights from design to diet.Nature reviews. Cancer · 2026Review
- Immune dysregulation and stem-like CD8+ T cell enrichment in type 1 diabetes pancreatic lymph nodes.The Journal of clinical investigation · 2026Article
- Aberrant immune regulation and enrichment of stem-like CD8bioRxiv : the preprint server for biology · 2026Article
- SLC7A5 regulates B cell metabolism and plasma cell differentiation independent of leucine transport.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Tissue Immunometabolism in Autoimmunity.European journal of immunology · 2026Review
- The cellular senescence-metabolism axis: emerging insights into T cell dynamics in the context of biological aging.Cell communication and signaling : CCS · 2025Review
- 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
- Mitochondrial protein OPA1 is required for the expansion of effector CD8 T cells.Cell reports · 2025Article
- Screening the human miRNA interactome reveals coordinated up-regulation in melanoma, adding bidirectional regulation to miRNA networks.Science advances · 2025Article
- Comprehensive analysis of disulfidptosis-related genes and the immune microenvironment in heart failure.Frontiers in cell and developmental biology · 2024Article
- Innate TCRβ-chain engagement drives human T cells toward distinct memory-like effector phenotypes with immunotherapeutic potentials.Science advances · 2023Article
- SRC2 controls CD4Proceedings of the National Academy of Sciences of the United States of America · 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
- SLC7A8 is a key amino acids supplier for the metabolic programs that sustain homeostasis and activation of type 2 innate lymphoid cells.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- cDC1 coordinate innate and adaptive responses in the omentum required for T cell priming and memory.Science immunology · 2022Article
- Mast cell surfaceome characterization reveals CD98 heavy chain is critical for optimal cell function.The Journal of allergy and clinical immunology · 2022Article
- Screening of ferroptosis-related genes in sepsis-induced liver failure and analysis of immune correlation.PeerJ · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
CD98 H chain (4F2 Ag, Slc3a2) was discovered as a lymphocyte-activation Ag. Deletion of CD98 H chain in B cells leads to complete failure of B cell proliferation, plasma cell formation, and Ab secretion. In this study, we examined the role of T cell CD98 in cell-mediated immunity and autoimmune disease pathogenesis by specifically deleting it in murine T cells. Deletion of T cell CD98 prevented experimental autoimmune diabetes associated with dramatically reduced T cell clonal expansion. Nevertheless, initial T cell homing to pancreatic islets was unimpaired. In sharp contrast to B cells, CD98-null T cells showed only modestly impaired Ag-driven proliferation and nearly normal homeostatic proliferation. Furthermore, these cells were activated by Ag, leading to cytokine production (CD4) and efficient cytolytic killing of targets (CD8). The integrin-binding domain of CD98 was necessary and sufficient for full clonal expansion, pointing to a role for adhesive signaling in T cell proliferation and autoimmune disease. When we expanded CD98-null T cells in vitro, they adoptively transferred diabetes, establishing that impaired clonal expansion was responsible for protection from disease. Thus, the integrin-binding domain of CD98 is required for Ag-driven T cell clonal expansion in the pathogenesis of an autoimmune disease and may represent a useful therapeutic target.
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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.