CD1d
- Known as:
- CD1d
- Catalog number:
- GTX11076
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CD1d
Related genes to: CD1d
- 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: CD1d
Related articles to: CD1d
- Y-box binding protein 1 (YB-1) is a multifunctional RNA- and DNA-binding protein with broad regulatory functions in gene expression, particularly at the posttranscriptional level. Here, we demonstrate that conditional deletion of YB-1 at the double-positive (DP) thymocyte stage causes an ∼80% reduction of invariant natural killer T (iNKT) cells in thymus, spleen, and liver, evident already in day-14 neonates and persisting into adulthood. Our data reveal CD44NK1.1 stage 1 accumulation and a selective loss of CD44NK1.1 stage 3 iNKT cells, indicating a postselection maturation defect. All iNKT cell subsets (iNKT1, iNKT2, iNKT17) were reduced, with thymic iNKT1 and splenic iNKT17 cells most severely affected. PMA/ionomycin-stimulated YB-1-deficient iNKT cells showed preserved IFN-γ/IL-4 frequencies but reduced per-cell cytokine production and a loss of IL-17 production. Interestingly, YB-1 DP thymocytes showed increased CD1d levels, suggesting increased TCR signal strength in the thymus of YB-1-deficient mice. Whereas CD5 levels were elevated, basal Nur77, ICOS, and CD122 (IL-15Rβ) expression were reduced in iNKT cells. Furthermore, apoptosis was increased, particularly at iNKT stages 2-3. Together, these findings identify YB-1 as a central regulator of iNKT cell development that integrates TCR, co-stimulatory, and IL-15 signaling to ensure postselection iNKT cell maturation, effector subset specification, and survival. - Source: PubMed
Schulze SilviaKnop LauraJantz-Naeem NouriaDovhan VladyslavaFricke StephanKahlfuß SaschaSchüler ThomasBommhardt Ursula - African swine fever virus (ASFV) is an important pathogen of domestic and wild suids and the causative agent of African swine fever (ASF). ASFV displays a tropism for myeloid cells, predominately of the monocyte/macrophage lineage, which is critical for ASFV pathogenesis. However, the mechanisms which govern the cellular tropism of ASFV are complex and incompletely understood. ASFV can enter susceptible cells through several mechanisms. One way is by clathrin-mediated endocytosis (CME) via interaction with the host glycoprotein CD1d, encoded by the gene, and disruption of expression significantly reduces ASFV replication in cell culture. In order to evaluate the role of CD1d in the replication and pathogenesis of ASF , knockout (KO) piglets generated using a CRISPR-Cas9 system were challenged with the highly virulent genotype II ASFV isolate MNG19. Remarkably, KO piglets were highly permissive to ASFV infection and developed severe acute ASF similar to age-matched wildtype (WT) controls. No significant differences in disease severity or mortality between ASFV-infected WT and KO pigs were observed. ASFV DNA levels in blood or in the majority of visceral and lymphoid tissues were also not significantly different between ASFV-infected wild-type and KO pigs. In addition, pathological changes were similar between both groups and typical of acute ASF such as fibrinous polyserositis, haemorrhagic lymphadenopathy, and systemic coagulopathy. This work demonstrates that porcine CD1d is not critical for genotype II ASFV replication and virulence , and that KO piglets possess no resistance to virulent genotype II ASFV infection. - Source: PubMed
Publication date: 2026/05/08
Madden DanielTrujillo Jessie DElango ShanmugasundaramFitz IsaacMcDowell Chester DAssato PatriciaLyoo EulimKwon TaeyongCool KonnerLi YonghaiFerreyra Franco MatiasGaudreault Natasha NMorozov IgorLee KihoDriver JohnRicht Juergen A - The mitogen-activated protein kinase (MAPK) pathways, ERK, JNK, and p38, are key regulators of immune responses during viral infections. These signaling cascades control cytokine production, T cell activity, and antigen presentation. However, many viruses can hijack MAPK pathways to avoid immune detection, promote their replication, and establish chronic infection. In this review, we discuss how different viruses, including HSV-1, HBV, HCMV, and SARS-CoV-2, manipulate MAPK signaling to alter host cell functions. A particular focus is given to the CD1d-iNKT cell axis, which plays a critical role in early antiviral responses but is often disrupted through MAPK-dependent mechanisms. We explore how changes in MAPK signaling affect antigen-presenting cells, drive T cell exhaustion, and reprogram immune cell metabolism, factors that contribute to viral immune evasion. The review also examines therapeutic strategies aimed at targeting MAPKs to improve antiviral immunity. These include small-molecule inhibitors and immune modulators that may enhance antiviral responses while limiting side effects. We emphasize the importance of context, as MAPK-targeted therapies must be carefully timed and tailored to avoid suppressing protective immunity or triggering unwanted inflammation. Overall, this review highlights the therapeutic potential and challenges of targeting MAPK pathways in viral infections and encourages further research into selective, host-directed antiviral strategies. - Source: PubMed
Publication date: 2026/04/03
Khan Masood AlamKhan Mohammad HamzaAllemailem Khaled S - Liver inflammation is a key driver of nonalcoholic fatty liver disease (NAFLD) and its progressive subtype, nonalcoholic steatohepatitis (NASH). Macrophages, as central players in the innate immune response, are crucial to disease pathogenesis; however, the upstream events that initiate their activation remain poorly defined. Here, we employed a cell-based chimeric receptor screening system and identified CD1d as a surface ligand for PIRA2. We subsequently demonstrated that CD1d stimulation activated macrophages both in vitro and in vivo. Co-immunoprecipitation assays further confirmed a direct interaction between CD1d and PIRA2. Using Pira2-deficient (Pira2) mice, we observed significantly reduced hepatic inflammation and lipid accumulation compared to wild-type controls. Importantly, macrophage-specific Pira2 conditional knockout mice similarly exhibited reduced macrophage activation and inflammatory cytokine production in vivo, confirming a macrophage-intrinsic role of PIRA2. Mechanistically, CD1d-PIRA2 interaction involves the α1 and α2 domains of CD1d and the D1 and D2 domains of PIRA2, leading to FcRγ ITAM tyrosine phosphorylation and downstream inflammatory signaling-events that are impaired in Pira2 macrophages. Additionally, CD1d and LILRA2 protein levels were elevated in NAFLD patients, and CD1d stimulation induced proinflammatory cytokine expression in human macrophages, which was attenuated by LILRA2 blockade. A recombinant LILRA2/Fc fusion protein effectively blocked CD1d-induced inflammatory gene expression in human macrophages, highlighting its potential as a therapeutic strategy for NAFLD. Collectively, our findings identify CD1d as a functional ligand of PIRA2 that promotes macrophage activation and inflammation, contributing to inflammatory progression in NAFLD. - Source: PubMed
Publication date: 2026/04/27
Tan XiaoshengLi QingwenMa ZhiboSun LingjuanZhao XiangliChen JianlinWang JingzengWeng XiufangChen LiChen ZhishuiLan Peixiang - Despite advances in treatment, chronic lymphocytic leukaemia (CLL) remains an incurable disease. Vδ1+ γδ T cells are reported to expand in CLL patients and to kill leukemic cells, placing them as candidates for immunotherapy. However, their cytotoxic efficacy was limited and required specific stimulatory conditions. Since some γδ T cells recognise lipids presented by CD1d, we examined if inducing CD1d expression and presentation of CD1d-restricted lipids could promote Vδ1, Vδ2 or Vδ3 T cell killing of B cells from CLL patients and healthy donors. Lines of γδ T cells containing Vδ1, Vδ2 and Vδ3 T cells and enriched cultures of CD19+ B cells were generated from peripheral blood using magnetic bead separation. γδ T cell subset frequencies and CD1d and ULBP3 expression levels on B cells were determined using flow cytometry. CD1d expression was induced on B cells by treatment with all trans retinoic acid (ATRA) and its analogue AM580. ATRA-treated B cells were co-cultured with γδ T cell lines in the absence or presence of lipids and cytotoxicity was assessed by measuring CD107a externalisation or propidium iodide staining using flow cytometry. Vδ1 and Vδ3 T cell frequencies were significantly higher in CLL patients compared to age-matched healthy donors. CD1d and ULBP3 expression was lower on CLL cells compared to healthy B cells but was restored by treatment with ATRA or AM580. Although co-culturing CLL cells with γδ T cells led to decreased cell viability, CD1d and ULBP3 upregulation by healthy and CLL B cells did not elicit cytolytic degranulation or cytokine production by Vδ1, Vδ2 or Vδ3 T cells, even after presentation of CD1d-restricted lipid antigens. This study suggests that human Vδ1 T cell cytotoxicity against CLL B cells may be disease stage-dependent and requires B cell priming and selective activation of specific γδ T cell subsets. - Source: PubMed
Publication date: 2026/04/20
David JulieWalsh AmySeow Ke SinWalsh EllenElekes StefanUpadhyay RohitTaher Nawal A BAl Siyabi SamihaMelo Ashanty MWaldron CarmelVandenberghe ElisabethMcElligott Anthony MDoherty Derek G