HLA_DQ (human) _ Clone FN81
- Known as:
- HLA_DQ (H. sapiens) _ Clone FN81
- Catalog number:
- T-1360.0100
- Product Quantity:
- 100ìg
- Category:
- -
- Supplier:
- New Immunology
- Gene target:
- HLA_DQ (human) _ Clone FN81
Related products to: HLA_DQ (human) _ Clone FN81
Related articles to: HLA_DQ (human) _ Clone FN81
- Psychiatric, neurodevelopmental, and neurodegenerative disorders, including Alzheimer's disease (AD), attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), bipolar disorder (BIP), major depressive disorder (MDD), and schizophrenia (SCZ), exhibit complex etiologies driven by immune and metabolic dysregulation. While distinct in their clinical onset, these conditions share overlapping molecular vulnerabilities. This study pioneers an integrative multi-omics framework, combining multi-tissue TWAS, cross-disorder pleiotropy analyses, Mendelian Randomization (MR), predictive machine learning, and BV2 microglial profiling. Crucially, our analysis uncovered a robust "Dual-Axis" etiological architecture. First, a systemic metabolic axis emerged as a primary driver, particularly involving FADS2-mediated lipid dysregulation and gut-brain axis interactions. This axis shares mechanisms between bipolar disorder and schizophrenia, with Multi-tissue TWAS revealing peripheral contributions (e.g., liver, colon) to CNS pathology. Second, MHC Class II-mediated pathways, driven by HLA-DRA, HLA-DRB1, HLA-DQB1, and HLA-DQA1, emerged as a transdiagnostic neuroinflammatory nexus across AD, BIP, MDD, and SCZ, orchestrating antigen presentation to CD4 T-helper cells. To bridge these genomic findings with cellular function, BV2 microglial profiling was performed to provide a cellular-context reference specifically for the identified immune risk component. This cellular model confirmed that the immunogenetic risk burden maps to a specific proinflammatory activation state characterized by upregulated neurotoxins (Lcn2, Nos2, Ccl2) and suppressed lipid transport/phagocytosis (Apoe, Cd68). Machine learning models leveraging these signatures achieved robust predictive performance, particularly for BIP and MDD. MR analyses uncovered causal roles of immune, lipid, and microbial pathways, with shared metabolic signatures (e.g., N-acetylarginine) across disorders. Integration with traditional medicine databases linked lipid metabolism to Artemisia argyi, suggesting novel therapeutic avenues. This integrative approach redefines the molecular framework of these disorders by highlighting systemic metabolic dysregulation and strongly implicating MHC Class II-mediated neuroinflammation as two convergent drivers, advancing precision psychiatry through targeted immunotherapies and metabolic modulators. - Source: PubMed
Publication date: 2026/07/14
Xu XuanFan Sha-ShaWu HaoDu YananBo YuHe JunwenHe YangCheng NaMeng Xiang-Yu - Preeclampsia (PE) is a leading cause of maternal and neonatal morbidity, with immune dysregulation at the maternal-fetal interface central to its pathogenesis. The highly polymorphic human leukocyte antigen (HLA) region mediates maternal immune tolerance of the semi-allogeneic fetus, yet the contribution of diversity to PE risk remains poorly defined. Whether the heterozygote advantage observed in other immune disorders is relevant to PE has not been systematically evaluated. Using data from the multi-ancestry TOPMed Boston-Colombia Collaborative for Adverse Pregnancy Outcomes (n = 12,790; 4,770 PE, 8,020 controls; 10,808 maternal, 1,982 fetal, including 1,848 pairs), we evaluated associations between heterozygosity across eight classical loci and PE and four sub-phenotypes, adjusting for genetic ancestry. heterozygosity was common across most loci (>80%). No individual maternal locus was associated with overall PE; however, heterozygosity across class I loci showed a protective effect in preterm PE (OR=0.82, 95%CI:0.69-0.97), with a similar pattern for heterozygosity (OR=0.78, 95%CI:0.64-0.96). In contrast, fetal heterozygosity at was nominally associated with increased risk of PE (OR=1.36, 95%CI:1.03-1.79) and preterm PE (OR=1.73, 95%CI:1.13-2.73). No individual maternal or fetal alleles were associated with PE. Maternal-fetal mismatch analysis demonstrated locus-specific associations with preterm PE, including increased risk with mismatch and reduced risk with mismatch. These findings highlight distinct maternal and fetal immunogenetic contributions to PE risk and underscore the importance of considering diversity-rather than individual alleles alone-in studies of PE etiology. - Source: PubMed
Publication date: 2026/06/18
Cao ChangMaher MatthewHu JieKeating Brendan JBurwick Richard MKarumanchi S AnanthMaxwell G LarryPowe Camille EMcElrath Thomas FCantonwine David ESerrano NormaColmenares ClaudiaCasas Juan PSaxena RichaGray Kathryn J - Lichen planus (LP) is an inflammatory disease affecting squamous epithelia, typically manifesting in a cutaneous (non-OLP) and an oral mucosa (OLP) form, the latter conferring elevated risk of oral squamous cell carcinoma. Despite the presence of CD4+ and CD8+ T-cell infiltrates in LP lesions, specific autoantibodies or target T-cell antigens have not been identified. A recent genome-wide association study (GWAS) uncovered 27 genome-wide independent associations, with the strongest signal within HLA Class II, particularly involving DQB1*05:01. This association showed stronger effects in non-OLP (OR = 2.09) versus OLP (OR = 1.36). Here, we performed a high-resolution HLA fine-mapping analysis in FinnGen to dissect this strong Class II signal and clarify its relationship to LP subtypes. We find that most DQA1*01~DQB1*05:01 haplotypes confer increased susceptibility, with the highest risk conferred by DQA1*01:05~DQB1*05:01 followed by DQA1*01:01~DQB1*05:01. In subjects not carrying DQB1*05:01, DRB1*15:01~DQA1*01:02~DQB1*06:02 had a strong protective effect, more pronounced in non-OLP than OLP. Further associations were found with DRB1*09:01 and DQB1*02:02 as well as independent HLA Class I associations with A*03:01, B*08:01 and B*13:02, all stronger in OLP versus non-OLP. Conditioning SNP associations for these effects eliminated the HLA GWAS signal. These effects highlight that while the DQB1*05:01 association remains largely invariant to DQA1 polymorphisms across LP subtypes, the variable strength of HLA associations in non-OLP and OLP forms suggests distinct immunopathological mechanisms. The presence of strong trans-heterodimer effects in this disease illustrates the need to analyse HLA-DQ-associated diseases with methods beyond simple conditioning. The invariance to DQA1 polymorphisms in LP may facilitate the identification of potential pathological epitopes. - Source: PubMed
Ritari JarmoReeve Mary PatFinnGen Maria SiponenVehviläinen MariSalo TuulaOsoegawa KazutoyoViña Marcelo FernandezGoudey BenjaminPartanen JukkaMignot Emmanuel J M - Mucinous adenocarcinoma (MAC) is a rare and clinically problematic subtype of rectal cancer, tending to present at an advanced stage and to respond poorly to neoadjuvant therapy. The consistently worse prognosis than that of not-otherwise-specified adenocarcinoma (NOS-AC) is not fully understood, potentially owing to intrinsically more aggressive biology or specific immune evasion mechanisms. We used the IMMUNOREACT multicentre cohort, with external validation in TCGA, to investigate the clinical and immunological features of rectal MAC in detail. - Source: PubMed
Publication date: 2026/06/15
Dell'Atti LorenzoKotsafti AndromachiGaluppini FrancescaScarpa MelaniaSalmaso RobertaStepanyan AstghikSbaraglia MartaSaadeh Luca MariaTussardi GaiaRosato AntonioAngriman ImerioRuffolo CesareUrso Emanuele Damiano LucaBao Quoc RiccardoNegro SilviaMaretto IsaccoFacci LucaRivella GiorgioD'Angelo AntonellaMatteazzi AnnaVignotto ChiaraBaldo AndreaGuzzardo VincenzaPellegrini ValerioBrignola StefanoCeccon CarlottaStecca TommasoPozza AnnaMassani MarcoDe Simoni OttaviaPilati PierluigiGruppo MarioFranzato BorisCataldo IvanaPortale GiuseppeCipollari ChiaraZuin MatteoLaurino LiciaDal Santo LucaPirozzolo GiovanniRecordare AlfonsoCeccarini LaviniaAntoniutti MicheleMarinelli LauraBrolese AlbertoBarbareschi MattiaBertalot GiovanniOrtenzi MonicaGuerrieri MarioZizzo MaurizioFabozzi MassimilianoGuerriero SilvioPiccioli AlessandraPozza GiuliaGodina MarioMondi IsabellaVerdi DauniaDa Lio CorradoNoaro GiuliaCola RobertoBordignon GiovanniMerenda RobertoBecherucci GiuliaGavagna LauraCandioli SalvatoreTagliente GiovanniTedeschi UmbertoParini DarioSalmaso BeatriceBusinello GianlucaCristofaro Loretta DiMarchegiani FrancescoBergamo FrancescaLonardi SaraPorzionato AndreaChiminazzo ValentinaScognamiglio FedericoBardini RomeoPucciarelli SalvatoreAgostini MarcoGregori DarioDi Camillo BarbaraCastagliuolo IgnazioSpolverato GayaFassan MatteoDei Tos Angelo PaoloScarpa Marco - The human leukocyte antigen (HLA) system is the primary determinant of donor selection in allogeneic hematopoietic cell transplantation (HCT) and plays a central role in solid organ transplantation, immune-mediated disease studies, evolutionary population genetics, and immunotherapy. Large-scale sampling of registry participants reflecting major US ancestry groups allows for characterization of the complex landscape of HLA haplotype diversity for the classical HLA class I (HLA-A, HLA-B, HLA-C) and HLA class II (HLA-DRB1, HLA-DRB3, HLA-DRB4, HLA-DRB5, HLA-DQA1, HLA-DQB1, HLA-DPA1, and HLA-DPB1) genes. Here we present nine-locus classical HLA allele and haplotype frequency estimates for five broad (Black, White, Asian or Pacific Islander, Hispanic and Native American) and 21 detailed US populations based on 9,671,082 donors with targeted genotyping by DNA-based methods. Frequency estimation used an expectation-maximization (EM) framework specifically adapted to handle mixed-resolution and ambiguous HLA genotyping data. Advancements in next-generation sequencing provide extensive HLA genotyping, offering new insights into the haplotype structure and diversity of the human MHC complex, expanding knowledge especially for HLA class II haplotypes. Population analyses reveal that the most common haplotypes are predominantly population-specific, with only three haplotypes shared across the top 100 lists of all five broad population groups, and that Black populations exhibit the greatest nine-locus haplotypic diversity, a pattern that persists after controlling for differences in registry sample size. These frequencies, derived from the largest US cohort to date, support clinical decision-making and research in histocompatibility, immunogenetics, and transplantation and are publicly available at https://zenodo.org/records/17966993. - Source: PubMed
Publication date: 2026/06/24
Gragert LorenMadbouly AbeerBashyal PradeepWadsworth KimKempenich JaneBolon Yung-TsiMaiers Martin