BTNL8 Antibody (Center)
- Known as:
- BTNL8 Antibody (Center)
- Catalog number:
- AP5012c
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- BTNL8 Antibody (Center)
Related genes to: BTNL8 Antibody (Center)
- Gene:
- BTNL8 NIH gene
- Name:
- butyrophilin like 8
- Previous symbol:
- -
- Synonyms:
- FLJ21458, BTN9.2
- Chromosome:
- 5q35.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-05
- Date modifiied:
- 2016-01-06
Related products to: BTNL8 Antibody (Center)
Related articles to: BTNL8 Antibody (Center)
- : Celiac disease (CD) is a T-cell-mediated autoimmune condition, triggered by gluten ingestion. Duodenal biopsy is the gold-standard diagnosis for CD, which is often limited by interobserver variability between pathologists. Immunohistochemistry (IHC) is a powerful technique for detecting biomarkers with potential diagnostic significance. This study aims to investigate five candidate biomarkers, BTNL8, NKp46, TdT, THEMIS, and TCRδ, that might improve the reproducibility of the diagnosis of CD. : Formalin-fixed paraffin-embedded material, surplus to diagnostic requirements, was obtained from 46 subjects (untreated CD: = 21, CD treated with gluten-free diet: = 5; controls: = 20) and immunostained for BTNL8, NKp46, TdT, THEMIS and TCRδ. BTNL8 staining was scored on a 0-3 semi-quantitative scale. NKp46, TdT, THEMIS, and TCR delta-positive intra-epithelial lymphocytes (IELs) were quantified as mean counts per 100 epithelial cells (ECs). : TCRδ-positive IELs were markedly elevated in CD biopsies (median 9.4 IELs/100 ECs) compared to healthy controls (median 0.5 IELs/100 ECs; < 0.001), with a threshold of >2.1 TCRδ-positive IELs per 100 ECs yielding an AUC of 0.94 and interobserver agreement of 0.82. NKp46 expression was also increased in CD (median 13.8 IELs/100 ECs) versus controls (median 9.6; < 0.001), with >12.8 NKp46-positive IELs per 100 ECs achieving an AUC of 0.86 and interobserver agreement of 0.82. Immunostaining for the other biomarkers demonstrated less clear differences between CD and healthy controls. : Corroborating several recent publications, TCRδ immunostaining provides high diagnostic accuracy and good interobserver agreement in the diagnosis of CD on duodenal biopsy, even for patients on a gluten-free diet. - Source: PubMed
Publication date: 2026/05/30
Lee HeeyeonShenoy VrindaGopalkaje PriyankaParsons SamKaistha AnuradhaSoilleux Elizabeth J - BACKGROUND: Transposable elements (TE) are mobile sequences in the human genome that change location, have variable expression and function as cis-regulating elements that modify the expression of the transcriptome. Based on the knowledge that the small airway epithelium (SAE) is the first site of early pathology caused by cigarette smoking, we hypothesized that smoking alters the expression of TE in the SAE and some smoker dysregulated SAE TE are associated with dysregulation of the SAE transcriptome. METHODS: RNA-Seq of cigarette smokers (n = 20) and nonsmokers (n = 26) and single cell RNA-seq (scRNA-seq) analysis of n = 3 smokers and nonsmokers all with normal lung function, was performed to quantify expression of TE. RESULTS: Compared to nonsmokers, cigarette smokers had 111 downregulated and 191 upregulated differentially expressed TE in the SAE. scRNA-seq showed that intermediate and differentiated club, mucus and ciliated cells had the highest number of dysregulated TE in smokers. Among the smoking-upregulated gene-TE pairs, genes involved in epithelial differentiation (EGF, MUCL1, MEP1A), immune responses and inflammation (IRGM, LUCAT1, LINCO1258), and tumorigenesis (AKR1B15). Conversely, smoking-downregulated gene-TE pairs included genes important for maintaining epithelial differentiation (DAPK1, CD81-AS1) and regulating immune functions (BTNL8, LTF, CFH, C4BPA, CCL17). Smoking-induced dysregulation of TE in the SAE of cigarette smokers in intermediate and differentiated cells was associated with dysregulation of genes in the SAE transcriptome. CONCLUSIONS: Understanding the impact of smoking on TE-mediated gene regulation may lead to the identification of new therapeutic targets for smoking-related lung diseases. - Source: PubMed
Publication date: 2026/03/17
Rostami Mahboubeh RStrulovici YaelKaner Robert JCrystal Ronald Gde Mulder Rougvie Miguel - 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 - Ulcerative colitis (UC) is an immune-mediated chronic inflammatory bowel disease, and with the rising global incidence and the risk of malignant transformation, the treatment of UC is challenged by heterogeneous progression and limited targeted therapies, and its underlying pathogenesis remains unclear. This study aims to identify novel therapeutic targets for UC, elucidate the genetic factors associated with UC development, and advance precision medicine strategies for UC. - Source: PubMed
Publication date: 2025/12/08
Zhu XiangYang YujieZhu Yi - 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