HLA-DQA2 Blocking Peptide
- Known as:
- Human leukocyte antigen-DQA2 Blocking Peptide
- Catalog number:
- 33r-5275
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- HLA-DQA2 Blocking Peptide
Related products to: HLA-DQA2 Blocking Peptide
Related articles to: HLA-DQA2 Blocking Peptide
- Chronic Rhinosinusitis (CRS) shares epidemiological links with Cardiovascular Diseases (CVDs), however, their shared genetic basis remains unclear. We hypothesized that pleiotropic genetic variants underlie CRS-CVDs links via distinct biological pathways. - Source: PubMed
Publication date: 2026/09/02
Wei BoHe JiaoyuGan WeigangWang BinbinLiu Feng - Gestational diabetes mellitus (GDM) is a major public health challenge characterized by placental immunometabolic dysregulation. This study aimed to identify molecular signatures associated with GDM-related placental pathology and evaluate their diagnostic and therapeutic implications. - Source: PubMed
Publication date: 2026/08/29
Liu ShuyuFeng JingxiangDing YoudeLiang Weizhang - Elevated intratumoral immune inflammation prior to treatment is typically associated with better outcomes in hot tumors treated with immune checkpoint inhibitors (ICIs). However, we observed a paradox in pMMR/MSS locally advanced rectal cancer (LARC) patients, where a subset with elevated baseline immune inflammation exhibited worse outcomes after combined radiotherapy and ICI treatment compared with patients with minimal immune inflammation. To investigate this counterintuitive finding, we performed paired scRNA-seq and scTCR-seq on longitudinally collected samples, including tumor biopsies (pre-treatment, post-radiotherapy, and post-immunotherapy) and peripheral blood mononuclear cells (pre-treatment and post-immunotherapy), from 20 pMMR/MSS LARC patients treated with sequential radiotherapy and ICI therapy (NCT06493240). We propose the concept of clonal entrapment to explain this phenomenon. Specifically, our profiling results reveal that increased HLA-DQA2 expression in dendritic cells and upregulated GDF15 expression in treatment-resistant tumor cells correlate with the restricted expansion of novel tumor-reactive TCR clonotypes. Consequently, the immune response is limited primarily by pre-existing TCR clonotypes within the tumor, especially those partially expanded under chronic inflammation, leading to the expansion of TCR clonotypes derived mainly from pre-treatment CD8 T cell pools following ICI therapy. By identifying this feature of the pMMR/MSS LARC microenvironment, our study provides a high-resolution framework for understanding resistance to sequential radiotherapy and ICI therapy. - Source: PubMed
Publication date: 2026/06/30
Tang ZhichunZhu MingxuanZhao ShidongPang DazhiCui YanchengLin GuoleWu AiwenLin YilinJiang XinyangZhang WeiXiong NanYang ChangjiangWang CaihongWang ShanYe YingjiangBai FanShen Zhanlong - Although it was proposed that cell fusion of cancer cells with leukocytes creates mobile hybrids with a metastatic phenotype, it has been difficult to genetically confirm cell fusion events in human cancer in vivo. Here, we experienced 4 cases of placental site trophoblastic tumor (PSTT) that produced immunoglobulin (Ig). Three cases showed recurrence and responded well to pembrolizumab therapy. Among them, we could analyze temporal changes in the genetic profiles on one case of daughter-derived PSTT, which relapsed after pembrolizumab therapy. In this case, we found that PSTT incorporated the exogenous genes from host maternal cells. The rearrangement patterns of Ig genes and protein expressions sequentially increased. By analyzing single-nucleotide variants, PSTT incorporated daughter-non-inherited maternal alleles (DNIMA), including the Ig lambda and HLA-DQA2 loci. Protein expressions of TLR10 and SIGLEC10 increased during tumor progression concomitantly with DNIMA incorporation. DNIMA mapping indicates the incorporation of exogenous maternal genes was widely distributed through the whole chromosomes, suggesting the involvement of cell fusion in gene transfer mechanisms. These findings indicate that PSTT sequentially incorporated exogenous genes from maternal cells to express immune-related molecules and suggest that cancer cells acquired B cell-related functions, including Ig production by cell fusion with host immune cells. - Source: PubMed
Publication date: 2026/06/23
Kagami KyosukeOno MasanoriMizumoto YasunariKanda TatsuhitoIizuka TakashiDaikoku TakikoHorike Shin-IchiHattori AkiraHorie AkihitoMinamiguchi SachikoFujiwara TomokoHosomichi KazuyoshiTajima AtsushiUsui HirokazuAbiko KaoruFujiwara Hiroshi - Coronavirus Disease 2019 (COVID-19) and other lower respiratory tract diseases (LRTDs), including bacterial pneumonia and acute respiratory distress syndrome, share overlapping clinical features but arise from distinct pathophysiological mechanisms. The molecular signatures that distinguish these diseases remain insufficiently characterized in African populations, where genetic background, endemic infections, and environmental exposures may substantially shape immune responses. We integrated spatially resolved single-cell transcriptomic profiles from lung autopsy specimens of 30 Malawian patients, including 10 with COVID-19, 12 with other LRTDs, and 8 non-LRTD controls. In total, 61,391 cells representing 15 cell types and 36,602 gene expression features were analyzed. Using an integrated machine learning framework that combined nine feature-ranking algorithms with incremental feature selection, we identified potential molecular signatures that could discriminate among disease states within this cohort. The optimal classification models achieved weighted F1 scores greater than 0.94, demonstrating a robust capacity to differentiate COVID-19 from other LRTDs in our dataset. Notably, the macrophage-associated state in COVID-19 was dominated by an IFN-γ response with upregulation of CD163 and HLA-DQA2, contrasting sharply with the type I/III interferon signature reported in European cohorts. In addition, we observed cell-type-specific COVID-19 signatures, including downregulation of CAV1 in AT1 cells, consistent with epithelial damage; dysregulation of SFTPC in AT2 cells, suggesting surfactant dysfunction; and upregulation of NFKBIA in neutrophils, indicating altered inflammatory regulation. Gene Ontology enrichment further revealed universal disruption of protein synthesis machinery, along with cell-type-specific alterations in immune activation, epithelial repair, and inflammatory signaling pathways. - Source: PubMed
Publication date: 2026/05/04
Bao YushengZhou XianchaoChen LeiFeng KaiyanGuo WeiHuang TaoCai Yu-Dong