Rabbit polyclonal to CD1d, Host Rabbit
- Known as:
- Rabbit pab CD1d, Host Rabbit
- Catalog number:
- YF-PA10744
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abfron
- Gene target:
- Rabbit polyclonal CD1d Host
Related genes to: Rabbit polyclonal to CD1d, Host Rabbit
- 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: Rabbit polyclonal to CD1d, Host Rabbit
guanine nucleotide binding protein alpha inhibiting activity polypeptide 1 (GNAI1) polyclonal antibody kinase suppressor of ras (KSR) polyclonal antibody'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(Alpha)_ 1 _ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_1_ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,β-cyclohexyl-Ala8,D-Tic16,Arg17,Cys18)-Atrial Natriuretic Factor (6-18) amide (mouse, rabbit, rat)
A71915 98% C69H116N26O15S2 CAS:(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Guinea Pig(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Guinea Pig(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Guinea Pig Related articles to: Rabbit polyclonal to CD1d, Host Rabbit
- Vγ9Vδ2-T cells form a conserved T-cell subset known for its potent intrinsic antitumor activity and versatility in recognizing diverse cancer types independently of the major histocompatibility complex. Previously, we reported the preclinical activity of a bispecific T-cell engager (bsTCE) specific for both CD1d and the Vδ2-TCR that engaged both Vγ9Vδ2-T and type 1 natural killer T cells to CD1d-expressing hematological malignancies, including multiple myeloma (MM) and acute myeloid leukemia (AML). Here, we evaluated whether various standard-of-care drugs for patients with MM and AML/myelodysplastic syndromes (MDS) affected the in vitro antitumor activity of CD1d-Vδ2 bsTCE-activated Vγ9Vδ2-T cells. - Source: PubMed
Publication date: 2026/06/28
de Jong MilonVeth MyrtheBrachtlová TerezaKing Lisa ASaura-Esteller JoséBechler Tamara Mvan Helden Pauline MAlhan CananLameris Roelandde Gruijl Tanja Dvan der Vliet Hans J - CD1d-restricted invariant natural killer (iNK) T cells are innate T cells known for their ability to shape adaptive immunity toward inflammation or immune-suppression via the rapid production of Th1-, Th2-, and Th17-type cytokines from corresponding iNKT subsets such as NKT1, NKT2, and NKT17. IL-10-producing invariant NKT cells, termed NKT10 cells, are thought to play an immunoregulatory role, but their potential clinical use remains underexplored. We characterized human NKT10 cells from cord-derived iNKT cells and investigated their therapeutic utility in allogeneic stem cell transplantation. Cord and cord-derived iNKT cells contained a high frequency of CD4CD25CD161FoxP3 iNKT cells and showed Th2/Th10-biased cytokine production upon antigenic stimulation. Accordingly, cord-derived iNKT cells displayed a distinct gene expression profile with upregulated genes related to NKT2, NKT10, and regulatory T cells compared with adult donor-derived iNKT cells. Furthermore, single-cell RNA sequencing analysis of cord-derived iNKT cells confirmed the presence of NKT10-like subset that was enriched with multiple immunoregulatory pathways and genes related to immune-checkpoints (, , , and ) and NKT10 (, , and ), whereas the NKT1/17-like subset present in adult donor-derived iNKT cells showed upregulation of genes related to cytotoxicity (, , and ), NKR (, , , and ), NKT1 ( and ), and NKT17 (). Lastly, cord-derived iNKT cells suppressed alloreactive T cell proliferation and ameliorated xenogeneic graft-versus-host disease where the immunodeficient NSG mice received human peripheral blood mononuclear cells supplemented with cord-derived iNKT cells. Thus, NKT10-enriched, cord-derived iNKT cells are candidate cell therapeutics for immune-modulation in allogeneic stem cell transplantation and other autoimmune diseases. - Source: PubMed
Publication date: 2026/06/10
Trujillo-Ocampo AbelBorges PamellaGrefe MaisonVaz de Freitas MartielaLee Sung-EunQi YuanClinton JelitaLi DanHe HongYu LingPeris-Cuesta ArnauEhli Erik AMa QingSu XiaopingAmaral Antunes DinlerAl-Atrash GheathMolldrem Jeffrey JShpall Elizabeth JIm Jin S - Nasopharyngeal carcinoma (NPC) is a subtype of head and neck squamous cell carcinoma characterized by high recurrence and metastasis rates and poor prognosis. Although immune checkpoint inhibitors have emerged as a promising treatment strategy for recurrent/metastatic nasopharyngeal carcinoma (R/M NPC), only a few patients have benefitted significantly from them. Lipid metabolism reprogramming plays a crucial role in NPC progression and its interaction with the immune microenvironment. This study aims to establish a prognostic model for NPC based on lipid metabolism-related factors, further explore its association with tumor immunity, and investigate the potential for immunotherapy. - Source: PubMed
Publication date: 2026/06/25
Xu YangZhu LiruZhang QingqingChen XiaojunLv HaoyuMa ShuhanWang RunzhiChang YuanyuanSun YongchuChen KaihuaLi LingZhu Xiaodong - Objective To investigate the early transcriptomic characteristics of neutrophils and monocytes stimulated by the major surface protein 2 (MSP2) of anaplasma phagocytophilum(AP), to preliminarily explore their functional differences and potential common pro-inflammatory mechanisms of these two cell types in the inflammatory response, and to provide a theoretical basis for understanding the inflammatory pathogenesis of Human Granulocytic Anaplasmosis (HGA) and for developing anti-inflammatory strategies. Methods HL60 cells (rHL60) differentiated with dimethyl sulfoxide (DMSO) for 8 days were used as a neutrophil-like cell model, and human acute monocytic leukemia (THP-1) cells were used as a monocyte model. Both cells were stimulated with recombinant MSP2 (rMSP2) for 2 hours. Differentially expressed genes (DEGs) were identified by transcriptome sequencing, and their biological functions and related signaling pathways were analyzed via Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment. The mRNA expression levels of key DEGs were validated by real-time quantitative PCR (qPCR), and the concentrations of cytokines in cell supernatants were measured by ELISA. Results Transcriptome analysis showed that in rHL60 cells, DEGs were mainly enriched in inflammation. qPCR confirmed the up-regulation of C-C motif chemokine receptor 7 (CCR7) and oxidized low-density lipoprotein receptor 1 (OLR1), while CD1D molecule and C-X-C motif chemokine receptors 1/2 (CXCR1/2) were down-regulated. In THP-1 cells, DEGs were primarily enriched in transcriptional regulation. qPCR validated the up-regulation of nuclear factor kappa B inhibitor zeta (NFKBIZ) and nuclear receptor subfamily 4 group A member 3 (NR4A3), whereas thioredoxin-interacting protein (TXNIP) and interleukin-16 (IL-16) were down-regulated. ELISA results demonstrated that both cell types significantly secreted C-C motif chemokine ligands 3/4/20 (CCL3/4/20) following MSP2 stimulation. Conclusion In the early phase of MSP2 stimulation, neutrophils serve as the primary cells initiating the inflammatory response, whereas monocytes focus on immune regulation. The co-secretion of CCL3, CCL4, and CCL20 may represent a potential molecular mechanism by which these two innate immune cell types jointly promote inflammatory responses during AP infection. - Source: PubMed
Chen ShihuaWang FengYue LeiYan Min - continuously sheds live organisms and persists in the large intestine following intracolonic inoculation, while the live-attenuated chlamydia oral vaccine intrOv, an IFNγ-susceptible mutant of , fails to do so. IFNγ delivered by group 3 innate lymphoid cells (ILC3s) have been shown to block intrOv shedding. We now report that mice deficient in lymphocytes but competent in ILCs allowed intrOv to persist, revealing a critical role of lymphocytes for preventing intrOv persistence. The responsible lymphocyte subsets are natural killer T cells (NKTs), as mice deficient in either CD1d or β2m permitted intrOv to persist. We further narrowed the responsible cells to invariant NKTs (iNKTs) that produce IFNγ, as mice deficient in TCRα J18 segment (Traj18), T-bet, or IFNγ failed to prevent intrOv persistence. Consistently, intrOv induced IFNγiNKTs, and wild-type iNKTs prevented intrOv persistence in mice deficient in either lymphocytes or IFNγ. Thus, IFNγiNKTs are both necessary and sufficient for preventing intrOv persistence, while IFNγILC3s are for blocking intrOv shedding, revealing a division of labor between IFNγiNKTs and IFNγILC3s in regulating the interaction of the obligate intracellular Chlamydia with host mucosal tissue. The information is also essential for improving the safety and efficacy of intrOv as an oral vaccine. - Source: PubMed
Publication date: 2026/06/01
Abdelsalam Ahmed MohamedWu YiKronenberg MitchellFan HuizhouZhong Guangming