Anti-Mouse CD1d Purified 100 ug
- Known as:
- Antibody toMouse CD1d Purified 100 ug
- Catalog number:
- 14-0011-82
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD1d Purified 100
Related genes to: Anti-Mouse CD1d Purified 100 ug
- Gene:
- CD1D NIH gene
- Name:
- CD1d molecule
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-11
- Date modifiied:
- 2015-08-27
Related products to: Anti-Mouse CD1d Purified 100 ug
Related articles to: Anti-Mouse CD1d Purified 100 ug
- Invariant natural killer T (iNKT) cells are unconventional ɑβ T cells that respond to lipid-based antigens. They play a vital role in response to infections and are involved in diseases such as allergic asthma and cancer. Despite clear immunological roles across multiple diseases, remarkably few tools exist to study iNKTs in vivo. In this study, we report that the Fgd5ZsGreen/+ reporter mouse widely used to study hematopoietic stem cells (HSCs) can dually serve to identify rare immune cell populations, including a subset of iNKTs. Specifically, we show that a "non-HSC" population of CD45+Fgd5ZsGreen+ cells reside in multiple organs including the lungs, liver, spleen, and thymus. The majority of these Fgd5ZsGreen+ cells do not express canonical HSC markers but instead express CD5. RNA sequencing of CD5+EPCR-Fgd5ZsGreen+ bone marrow cells showed greatest similarity to iNKT cells, and these findings were corroborated by additional cell surface marker analysis of TCRβint CD1d-PBS57+ iNKT cells in reporter mouse tissues. We found that roughly 20% of total thymic iNKT cells were Fgd5-ZsGreen+ and that these cells predominantly coexpressed NK1.1 and CD122, consistent with an iNKT1 cell phenotype. Transcriptomic and proteomic profiling of sorted Fgd5-ZsGreen- and Fgd5-ZsGreen+ iNKT cells revealed a number of key genes involved in cytotoxic responses as distinct between the two iNKT cell populations. These different cytotoxic profiles were further supported by cytokine expression following stimulation, indicating the potential existence of disparate iNKT1 subsets. Together, these data implicate Fgd5 expression as a powerful new tool for phenotyping and tracking cytotoxic iNKT1 cell subsets in vivo. - Source: PubMed
Cull Alyssa HChe James Lok ChiMacDonald SandyJassinskaja MariaHogg AlexanderGonka MonikaDavey JohnBennett EllieElberfeld SamuelVasey GraceBelmonte MiriamOedekoven Caroline ABode DanielColborn Lauren BMai CeraZwart MikaGreenman JoannaDann EmmaSuo ChenquLeborgne Nathan G FBoucher DaveTeichmann SarahLo Celso CristinaLaurenti ElisaHewitson James PKent David GBarlow Jillian L - Myeloid cells play crucial roles in cancer progression, influencing tumor growth, metastasis, and response to immunotherapy. The mechanisms shaping their diverse functions in the tumors remain poorly understood and may offer therapeutic opportunities. Here, we identify the lipid-presenting molecule CD1d as a regulator of tumor progression and myeloid heterogeneity in the tumor microenvironment. Using several mouse models of breast cancer, we demonstrate that genetic deletion or antibody-mediated targeting of CD1d leads to reduced tumor growth, altered immune infiltration, and improved efficacy of anti-PD-1 immunotherapy. Specifically, CD1d targeting reshapes the intratumoral myeloid compartment, enhancing proinflammatory programs and resulting in accumulation of inflammatory monocytes. The CD1d-dependent control of myeloid cell functional differentiation is cell-intrinsic and conserved in human and mouse. Through single-cell RNA sequencing, we define the transcriptional landscape associated with CD1d deficiency and derive a gene signature that correlates with clinical outcomes and response to immunotherapy in breast cancer patients. Thus, CD1d could provide a potential target to alter tumor-infiltrating myeloid populations and enhance immunotherapy responses. - Source: PubMed
Publication date: 2026/08/13
Evans LaurenConde Poole MariaCelik CenkMishra HarshitaPitcher Michael JGrigoriadis AnitaSecrier MariaBarral Patricia - This study examines sulfamethoxazole (SMX), a sulfonamide antibiotic strongly associated with severe cutaneous adverse effects, as a potential regulator of invariant natural killer T (iNKT) cells. This work combines molecular docking (to evaluate the likelihood of SMX binding to residues within a conventional binding pocket), molecular dynamics (to assess the stability of SMX binding and the forces that may destabilize the interaction), flow cytometry (to evaluate iNKT-cell activation in the presence of SMX within the context of established antigen presentation models), and particularly Raman spectroscopy (to investigate whether SMX-associated spectral features are retained after co-incubation and interaction) directly on sorted iNKT cells. Functional activation was assessed through IFN-γ production from sorted iNKT cells and correlated with Raman spectral data to support our hypothesis. The Raman spectroscopy was performed on both CD1d dimer (in isolation) as the presenter molecule of the drug and in sorted iNKT cells (in isolation), to identify spectroscopic evidence of drug-CD1dimer or drug-cell interactions under near-physiological conditions. From the CD1d experiment, we observed spectral features consistent with potential interactions between CD1d and serum-derived lipids, in a manner comparable to the positive control (α-GalCer). From the iNKT experiment, peaks at 1610 and 1663 cm-1 are the representative peaks that emerge under SMX stimulation conditions in iNKT cells (through TCR binding), as identified by second principal component (PC2) analysis. From the complete experiment, (CD1d + iNKT) suggests the possibility of a direct interaction between SMX and iNKT TCRs. Flow cytometry analysis further demonstrated a significant increase in ZAP-70 phosphorylation in sorted iNKT cells exposed to SMX under serum-free conditions, supporting the possibility of proximal TCR-associated signaling in the absence of CD1d. - Source: PubMed
Hernández-Jaimes O AZárate-Reyes J MLópez-Luis M AOrtiz-Sánchez EGallardo-Hernández S - BTNL3 and BTNL8, butyrophilin-like (BTNL) family receptors, are predominantly expressed on intestinal epithelial cells. The BTNL3-BTNL8 complex selectively activates human Vγ4⁺ T cells, which play critical roles in intestinal immune homeostasis and tissue damage repair. Here, we report the structure of the BTNL3-BTNL8-Vγ4Vδ1 T cell receptor (TCR) complex. The structure reveals that BTNL3-BTNL8 forms an antigen-independent tetramer, in contrast to the phosphoantigen-driven association of BTN2A1-BTN3A1. Two BTNL3-BTNL8 heterodimers clamp a head-to-head TCR homodimer to form a 2:2:2 BTNL3:BTNL8:Vγ4Vδ1 TCR complex, with the Vγ4 HV4 and CDR2 loops jointly engaging BTNL3. Structural alignment indicates that the CD1d binding site on TCR overlaps spatially with one monomer within a TCR dimer, suggesting that TCR dimerization sterically precludes simultaneous engagement of CD1d molecules. Together, our results elucidate the structural mechanism of BTNL3-BTNL8-mediated engagement and activation of Vγ4Vδ1 TCR, offering insights into γδ TCR signaling initiation. - Source: PubMed
Publication date: 2026/08/03
Dong DeLi HuilingZhu YuweiLu ZebinZhu JunliangTian XinyuHuang Zhiwei - Invariant natural killer T (iNKT) cells are innate-like lymphocytes that rapidly respond to lipid antigens presented by CD1d or to inflammatory cytokines and influence diverse immune responses. Much of our current understanding of iNKT cell biology derives from murine studies, which established a framework of thymic differentiation into NKT1, NKT2, and NKT17 subsets. Recent single-cell RNA sequencing (scRNAseq) studies have substantially expanded this view by revealing non-linear developmental trajectories, early epigenomic priming, and a multipotent recent thymic emigrant population that continues to differentiate after thymic egress. In peripheral tissues, iNKT cells undergo extensive remodeling driven by local environmental cues and antigen exposure, giving rise to regulatory, and effector states not observed in the thymus. At the same time, emerging human studies reveal principles that differ from those described in mice. Human iNKT cells exhibit a blended type 1/type 17 transcriptional program, limited evidence for NKT2-like populations, and functionally distinct CD4+, double-negative (DN), CD8αα+, and terminal effector-like subsets. Comparative analyses across species further suggest that differences in thymic selection, transcription factor networks, and peripheral maturation contribute to divergent patterns of iNKT cell specialization. Together, these findings support a revised view of iNKT cells as dynamic and context-dependent transcriptional states shaped by developmental history, tissue environment, antigen exposure, and species-specific regulatory programs. - Source: PubMed
Publication date: 2026/07/15
Zhao MengWu Lihua