ArticleCell reports2022
Antigen-presenting T cells provide critical B7 co-stimulation for thymic iNKT cell development via CD28-dependent trogocytosis.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- A CARMIL2 gain-of-function mutation suffices to trigger most CD28 costimulatory functions in vivo.The Journal of experimental medicine · 2025Article
- Intercellular Transfer of Immune Regulatory Molecules Via Trogocytosis.Results and problems in cell differentiation · 2024Review
- CTLA4 depletes T cell endogenous and trogocytosed B7 ligands via cis-endocytosis.The Journal of experimental medicine · 2023Article
- Impaired thymic iNKT cell differentiation at early precursor stage in murine haploidentical bone marrow transplantation with GvHD.Frontiers in immunology · 2023Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Invariant natural killer T (iNKT) cell development in the thymus depends on T cell receptor recognition of CD1d ligand on CD4/CD8 double-positive thymocytes. We previously reported that B7-CD28 co-stimulation is required for thymic iNKT cell development, but the cellular and molecular mechanisms underlying this co-stimulatory requirement are not understood. Here we report that CD28 expression on CD1d-expressing antigen-presenting T cells is required for thymic iNKT cell development. Mechanistically, antigen-presenting T cells provide co-stimulation through an unconventional mechanism, acquiring B7 molecules via CD28-dependent trogocytosis from B7-expressing thymic epithelial cells, dendritic cells, and B cells and providing critical B7 co-stimulation to developing iNKT cells. Thus, the present study demonstrates a mechanism of B7 co-stimulation in thymic T cell development by antigen-presenting T cells.
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Registered trials
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