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
- 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 - Neoadjuvant chemoradiotherapy (nCRT) is the main treatment for Locally Advanced Rectal Cancer (LARC). The response to nCRT varies from a complete response to no response. The impact of the B cells in this process is poorly understood. This study aimed to characterize the B cells types associated with response or resistance to nCRT. We applied the "Scissor" algorithm to integrate single-cell RNA-seq data with bulk transcriptome data from colorectal cancer samples, thereby identifying B cell subpopulations associated with nCRT response and exploring the clinical significance of B cell-related characteristic genes in nCRT for rectal cancer. At the single-cell level, we identified a B cell subpopulation characterized by the expression of HLA-DRB5, HLA-DQA2, HLA-DQB1, CD74, and ACTG1, which was associated with nCRT response in rectal cancer. Using subpopulation-specific trait genes, rectal cancer patients were classified into three distinct subtypes with unique features. Subtype A shows higher PD-L1 expression suggesting that patients in this subgroup are more likely to achieve favorable responses to immunotherapy. Subtype C shows lower hypoxia scores and a higher proportion of patients deriving clinical benefit from nCRT, suggesting that this subgroup may be more sensitive to neoadjuvant treatment. We developed a machine learning-based predictive model for pathological complete response (pCR) to nCRT in rectal cancer, achieving an area under the curve (AUC) of 0.911 in the training set and 0.819 in the 64-sample validation cohort. This study reveals that a B cell subpopulation characterized by the co-expression of HLA-DRB5, HLA-DQA2, HLA-DQB1, CD74, and ACTG1 is significantly associated with nCRT response in rectal cancer. These findings offer actionable insights for optimizing clinical treatment strategies, including patient stratification and personalized therapy selection. - Source: PubMed
Publication date: 2026/01/02
Xia HuangLin YuLi ZeyuanZeng LijingYao QiweiXu BenhuaZheng Rong - Immune dysfunction and systemic inflammation are hallmarks of decompensated liver cirrhosis (DLC), associated with an increased risk of developing sepsis. Rapid immune degradation is poorly understood in DLC patients; therefore we performed single-cell RNA (scRNA) transcriptomics in DLC patients. Twenty-one DLC patients (all males, 42 ± 7 year) with sepsis ( = 10) and without sepsis (w/o, = 11) and ten healthy controls PBMCs, were analysed for scRNA transcriptomics using the BD Rhapsody. Cell clustering and cell types were determined using gene expression data and validation of specific genes was done by qRT-PCR. Retrospectively analyzed proteomics data from same patients was used for RNA-Protein interactions. Ten clusters and 7 cell types were detected, with high heterogeneity in the monocyte cluster in DLC patients. All DLC patients irrespective of sepsis showed down regulation of O6-methylguanine-DNA methyltransferase (MGMT) mediated DNA damage reversal, mitochondrial transcription termination, and melanin biosynthesis, with upregulated lactose synthesis, hydroxycarboxylic acid, FGFR1b and FGFR1c receptors. DLC-sepsis showed down regulation of NF-kβ, TNF-α, and IL-17 signaling in classical monocytes compared to w/o sepsis. Serotonin and DNA repair genes were significantly increased in DLC sepsis ( < 0.05). In addition to HLA-DR, HLA-A, HLA-B, and HLA-DQA1 were also decreased but HLA-DRB1, HLA-C, HLAE, HLA-DRA, and HLA-DQA2 were raised in sepsis. RNA-protein interaction revealed the down regulation of PROS1, CDC42, CD62L, FCGR3B, CX3CR1, Rpl31 genes in sepsis. Chances of sepsis increased in DLC patients due to monocytic defects in genes and signaling pathways. These markers further can be explored for diagnostic purposes and early detection of sepsis. - Source: PubMed
Publication date: 2025/12/30
Sehgal RashiGautam PramodIslam MojahidulKumar Sevak JayeshJaved MaryamKaur NavkiranRamakrishna GayatriMaiwall RakhiSarin Shiv KumarTrehanpati Nirupama