ArticlePloS one2016
CRISPR-Mediated Slamf1Δ/Δ Slamf5Δ/Δ Slamf6Δ/Δ Triple Gene Disruption Reveals NKT Cell Defects but Not T Follicular Helper Cell Defects.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- The hyperinflammatory spectrum: from defects in cytotoxicity to cytokine control.Frontiers in immunology · 2023Review
- Current insights in mouse iNKT and MAIT cell development using single cell transcriptomics data.Seminars in immunology · 2022Review
- Development of αβ T Cells with Innate Functions.Advances in experimental medicine and biology · 2022Article
- SLAM family receptors control pro-survival effectors in germinal center B cells to promote humoral immunity.The Journal of experimental medicine · 2021Article
- Critical Role for SLAM/SAP Signaling in the Thymic Developmental Programming of IL-17- and IFN-γ-Producing γδ T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Regulatory Effect of Sishen Pill on Tfh Cells in Mice With Experimental Colitis.Frontiers in physiology · 2020Article
- SLAM-SAP-Fyn: Old Players with New Roles in iNKT Cell Development and Function.International journal of molecular sciences · 2019Review
- Review
- The Protein Phosphatase Shp1 Regulates Invariant NKT Cell Effector Differentiation Independently of TCR and Slam Signaling.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- SLAM receptors foster iNKT cell development by reducing TCR signal strength after positive selection.Nature immunology · 2019Article
- Ly9 (SLAMF3) receptor differentially regulates iNKT cell development and activation in mice.European journal of immunology · 2018Article
- Dissection of SAP-dependent and SAP-independent SLAM family signaling in NKT cell development and humoral immunity.The Journal of experimental medicine · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
SAP (SH2D1A) is required intrinsically in CD4 T cells to generate germinal center responses and long-term humoral immunity. SAP binds to SLAM family receptors, including SLAM, CD84, and Ly108 to enhance cytokine secretion and sustained T cell:B cell adhesion, which both improve T follicular helper (Tfh) cell aid to germinal center (GC) B cells. To understand the overlapping roles of multiple SLAM family receptors in germinal center responses, Slamf1Δ/Δ Slamf5Δ/Δ Slamf6Δ/Δ triple gene disruption (Slamf1,5,6Δ/Δ) mice were generated using CRISPR-Cas9 gene editing to eliminate expression of SLAM (CD150), CD84, and Ly108, respectively. Gene targeting was highly efficient, with 6 of 6 alleles disrupted in 14 of 23 pups and the majority of alleles disrupted in the remaining pups. NKT cell differentiation in Slamf1,5,6Δ/Δ mice was defective, but not completely absent. The remaining NKT cells exhibited substantially increased 2B4 (SLAMF4) expression. Surprisingly, there were no overt defects in germinal center responses to acute viral infections or protein immunizations in Slamf1,5,6Δ/Δ mice, unlike Sh2d1a-/- mice. Similarly, in the context of a competitive environment, SLAM family receptor expressing GC Tfh cell, GC B cell, and plasma cell responses exhibited no advantages over Slamf1,5,6Δ/Δ cells.
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Registered trials
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