Ask about this productRelated genes to: BTNL8 antibody
- 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
Related articles to: BTNL8 antibody
- 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. - 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 - Multisystem inflammatory syndrome in children (MIS-C) is a rare condition associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and characterised by systemic inflammation and T-cell dysfunction. A subset of patients with MIS-C were found to harbour rare variants in the gene BTNL8 that disrupt BTNL8-BTNL3 heterodimer formation, likely leading to inadequate γδ T-cell regulation and subsequent disrupted gut homeostasis. MIS-C shares clinical features with Kawasaki disease and similar mechanisms of pathogenesis with inflammatory bowel disease, despite these diseases being clinically distinct entities. We explore the common link between these diseases: the potentially critical role gut immunity plays in the initiation and persistence of disease through the tight regulation of γδ T cells via BTNL8 and BTNL3. Understanding the role of BTNL8 in the context of the overlap between these conditions may aid preventative measures and treatment of these conditions. - Source: PubMed
Publication date: 2025/09/18
Santillo DilysBellos EvangelosSancho-Shimizu Vanessa