BTNL3 antibody (FITC)
- Known as:
- BTNL3 (anti-) (fluorecein)
- Catalog number:
- orb4172
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- BTNL3 antibody (FITC)
Related genes to: BTNL3 antibody (FITC)
- Gene:
- BTNL3 NIH gene
- Name:
- butyrophilin like 3
- Previous symbol:
- -
- Synonyms:
- BTNLR, BTN9.1
- Chromosome:
- 5q35.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-08-22
- Date modifiied:
- 2016-10-05
Related products to: BTNL3 antibody (FITC)
Related articles to: BTNL3 antibody (FITC)
- 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 - Severe burns provoke a systemic "genomic storm," yet cell states associated with divergent outcomes remain unclear. We profiled blood cells by single-cell RNA-Sequencing (73,014 cells) from adult burn patients within post-burn day 17 (n=4) and healthy donors (n=5), integrated data with bulk signatures of burn size, inhalation injury, and mortality, and evaluated clinical associations in the ABA National Burn Repository. Burn was associated with emergency hematopoiesis marked by expansion of hematopoietic stem/progenitor-like cells, immature neutrophils, and plasmablast/plasma cell states, alongside depletion of naïve CD4+/CD8+ T cells and dendritic cells. Larger burns (>20% TBSA) showed enrichment of humoral transcriptional programs, including plasmablast/plasma cell activation and suppression of cytotoxic CD8+ T-cell states. In multivariable models, inhalation injury was a stronger predictor of death (adjusted OR 1.9) than burn size (adjusted OR 1.1) and shared greater overlap with the most perturbed single cells in non-survivors; 55% of co-perturbed cells were neutrophils, implicating granulocyte dysregulation as a common lethal axis. We identified a neutrophil-specific 5-gene panel (OLFM4, RETN, LCN2, ARG1, BTNL3) that discriminated survivors vs non-survivors after burns (AUC >0.9) and generalized to trauma (n=158; AUC 0.81) and ICU COVID-19 (n=103; AUC 0.75), providing information orthogonal to conventional biomarkers and severity scores. Cytomorphology corroborated transcriptomic immaturity, with ~2-fold higher band neutrophils and larger neutrophil size in a fatal case. Computational drug-reversal analysis highlighted galectin-1 inhibition as a candidate modulator of mortality-associated neutrophil programs. Together, our findings suggest that immature neutrophils represent a shared immune feature across severe burns and other forms of critical illness. Structured Abstract Objective: To define cell-specific immune programs associated with burn size, severity, inhalation injury, and fatal trajectories. - Source: PubMed
Publication date: 2026/04/29
Sinha SarthakMandujano-Tinoco Edna AyerimKutluberk ErenMulder Patrick P GCollao NicolásChockalingam KeerthanaPun AlexanderDardari RkiaVerly MyriamFraulin Frankie O GHarrop A RobertsonRosin Nicole LGabriel VincentBiernaskie Jeff - γδ T cells maintain intestinal immune homeostasis, but their contributions to human ulcerative colitis (UC) are poorly understood. We characterized γδ T cells in intestinal biopsies obtained from patients with UC and healthy donors using single-cell RNA sequencing, T cell receptor profiling, and mass cytometry. UC reduced CD103Vγ4Vδ1 γδ intraepithelial lymphocytes (γδ IELs) and increased γδ T cell subsets with stemlike phenotypes expressing TCF-1 (T cell factor 1) and PD-1 (programmed cell death receptor 1) or effector-like phenotypes expressing granzyme B, perforin, and T-bet in the lamina propria. γδ T cell composition changes in UC correlated with decreased expression of epithelial and and increased and , suggesting altered recruitment and activation. Clinical improvement recovered γδ IELs and reduced inflammation-associated subsets. Inflammation-associated changes were observed in peripheral blood γδ T cells. Thus, distinct γδ T cell subsets in different niches exert protective or pathogenic functions in UC. - Source: PubMed
Publication date: 2026/02/06
Mayer Lena SArnold JakobRoettele FelixReuter NadinePattekar AjinkyaOhtani TakuyaRibeiro Mariana MSiwicki RebeccaBruder KerstinObwegs DavidStahl ElinBuechel SarahRoehlen NataschaKolter JuliaMansoori Moghadam ZohrehAlaswad AhmedZhumalidova ZhibekLi GuangLiu XinjuanLi YangSingh AmitVillacorta Hidalgo JoseParaskevopoulou Maria DYajnik VijayJuarez JuliusRen YueLi HongzheWherry E JohnLewis James DWu Gary DBewtra MeenakshiTomov Vesselin TThimme RobertBengsch BertramHasselblatt PeterPicelli SimoneHofmann MaikeSagar - Multiple sclerosis (MS) is a chronic autoimmune disorder with a complex interplay of genetic and environmental factors. The familial aggregation of MS cases, especially within genetically related families, suggests a strong genetic component with high penetrance. This study explores the genetic factors contributing to MS in two multiclient MS families. Whole exome sequencing (WES) was performed on affected and unaffected members of the two multi-incident MS families with a history of genetic homogeneity. Selected variants were validated using appropriate molecular methods and linkage analysis under an autosomal recessive model. In silico analyses including protein modeling with AlphaFold3 and molecular docking using HADDOCK2.4, were conducted to evaluate the functional impact of the identified variants. Our study revealed two co-segregating copy number variants (CNVs) in BTNL3 and BTNL8 genes in one family. In silico modeling showed that the BTNL8*3 fusion protein, resulting from the identified CNVs, exhibited reduced binding affinity with the Vγ4 T-cell receptor (TCR). Comparison of the binding affinity between the BTNL8-BTNL3 heterodimer and BTNL8*3 fusion protein with Vγ4 TCRs revealed HADDOCK scores of -23.8 ± 4.8 and 8.8 ± 9.2, respectively, suggesting altered T-cell activation and a potential role in MS pathogenesis. A rare MBL2 variant (p.Pro101Leu) was also found in the second family, though its incomplete segregation with the MS phenotype suggests it may act as a genetic modifier. This study underscores the importance of both single-nucleotide variants and copy number in familial MS. The segregation pattern and characteristics of the identified variants in BTNL3 and BTNL8 support their potential association with disease risk. The BTNL8*BTNL3 fusion may influence γδ T cell selection and MS pathogenesis, warranting further functional studies. - Source: PubMed
Publication date: 2025/12/01
Torabi-Rahvar MonirehTalebi SaeedSalehi NajmehSahraian Mohammad AliSalehi ZahraIzad Maryam - The study aimed to investigate the prognostic significance of efferocytosis-related genes in ovarian cancer (OC) with regard to cancer development, progression, invasion, and metastasis. OC cohorts were assembled from bioinformatics repositories. Utilizing consensus clustering analysis, distinct clusters were delineated based on the intersection of OC-related genes and efferocytosis-related genes. A prognostic signature specific to efferocytosis in OC was developed using data from The Cancer Genome Atlas, validated against the gene expression omnibus database, and subjected to independent prognostic analysis. Subsequently, a nomogram model was formulated. Moreover, investigations encompassed the immune microenvironment, immunotherapy, mutation profiling, drug sensitivity assessments, drug prediction models, and molecular docking analyses. Finally, quantitative reverse transcription polymerase chain reaction (qRT-PCR) assays were employed to ascertain the mRNA expression levels of key genes. Five key genes, FCGBP, BTN3A3, WDR91, SLC25A45, and BTNL3, were identified as significantly associated with OC. Both datasets and qRT-PCR demonstrated elevated expression levels of FCGBP and WDR91 in OC. Notably, AFLATOXIN B1 exhibited strong binding affinity to SLC25A45, ciclopirox to BTN3A3, and irinotecan to WDR91. The risk score, age, and stage were identified as independent prognostic factors, with the nomogram displaying efficacy in predicting OC patient survival. Variations in the immune cell infiltration profiles, including naive B cells, and expression levels of 6 immune checkpoint genes, such as CTLA4, were notable. High tumor mutation burden scores were associated with improved survival outcomes. Additionally, significant differences in the IC50 values of 123 anticancer drugs were observed between the 2 risk groups. This findings of this study highlight the efficacy of the efferocytosis-associated risk model in predicting the survival outcomes of OC patients, thus providing a novel reference for prognostic prediction in OC patients. - Source: PubMed
Yuan XiaoqingHu YajunLi NaHe PeiWang DonghuaLiu YanLuo Yajuan