TIMD3 _ TIM3 _ HAVCR2 Antibody
- Known as:
- TIMD3 _ TIM3 _ HAVCR2 Antibody
- Catalog number:
- 10390-MM04
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- TIMD3 _ TIM3 HAVCR2 Antibody
Ask about this productRelated genes to: TIMD3 _ TIM3 _ HAVCR2 Antibody
- Gene:
- HAVCR2 NIH gene
- Name:
- hepatitis A virus cellular receptor 2
- Previous symbol:
- -
- Synonyms:
- Tim-3, TIM3, FLJ14428, TIMD3, CD366
- Chromosome:
- 5q33.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-12-04
- Date modifiied:
- 2018-06-27
Related products to: TIMD3 _ TIM3 _ HAVCR2 Antibody
Related articles to: TIMD3 _ TIM3 _ HAVCR2 Antibody
- - Source: PubMed
Publication date: 2026/08/19
Katano RuiShiratori SouichiTsuneta SatonoriTada Atsushi - Neonatal sepsis remains a leading cause of infant mortality, yet mechanisms driving concurrent hyperinflammation and immunosuppression remain unclear. Here, we perform single-cell RNA sequencing on 26 blood samples from 18 neonates, spanning acute sepsis, convalescence, and healthy controls. We identify 57 cell subtypes, revealing acute lymphoid depletion and myeloid expansion. S100A8 myeloid-derived suppressor cell-like (MDSC-like) cells represent a putative cytokine-storm source, potentially amplified by a feedforward S100-TLR4-MYD88 circuit. Innate-like lymphocytes fail to expand, succumbing to apoptosis and exhaustion despite heightened cytotoxicity. CD4 T cells display mitochondrial dysfunction, while regulatory T cells acquire a hyper-suppressive phenotype via the LGALS9-HAVCR2 axis. CD8 T cells undergo interferon-driven, innate-like reprogramming before lapsing into exhaustion, and B cells shift toward stress-adaptive, tolerogenic states. Together, our atlas defines a dual pathology in which MDSC-like cell-driven cytokine storm coexists with multi-lineage immunoparalysis, nominating the S100-TLR4 axis and mitochondrial dysregulation as potential therapeutic targets. - Source: PubMed
Publication date: 2026/08/24
Wang JieChen YingZou PeicenDu YueLi YingZhang LiZhou JuanWan LinglongXu YifeiWang YiWang YajuanMeng Lihui - Mendelian randomization (MR) is an important tool for identifying potential biomarkers and drug targets. Colocalization analysis is crucial for validating MR findings and guarding against confounding due to linkage disequilibrium. We aim to benchmark the performance of four Bayesian colocalization methods in validating MR-based target discoveries from circulating proteins for cardiometabolic traits. We assessed the associations between circulating levels of 1535 proteins and five cardiometabolic traits, followed by colocalization analyses using coloc, coloc+SuSiE, PWCoCo and SharePro. All methods demonstrated well-controlled false discoveries. SharePro demonstrated the highest frequency in supporting 160 (79.6%) of the 201 Bonferroni-significant protein-trait associations identified by MR, compared to coloc (supporting 40.3% of these associations), coloc+SuSiE (46.8%), and PWCoCo (45.8%), and was robust to varying prior colocalization probabilities. Protein-trait associations supported by SharePro were more likely to agree with significant gene-level associations identified in exome-wide association studies and implicate known drug targets. Eight protein-trait associations were exclusively supported by SharePro, suggesting potential cardiometabolic biomarkers or drug targets, such as HSF1 and HAVCR2. In summary, SharePro most often supports statistically significant associations identified through MR for cardiometabolic traits. Combining multiple lines of evidence using different methods may substantially increase the yield of biomarker and drug target discovery programs. - Source: PubMed
Publication date: 2026/08/18
Zhang WenminYoshiji SatoshiSladek RobertDupuis JoséeLu Tianyuan - Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by immune dysregulation. Tim-3 is an immune checkpoint receptor implicated in various autoimmune conditions. This study aimed to evaluate Tim-3 expression across monocyte subsets in newly diagnosed, treatment-naive SLE patients and assess its clinical relevance and diagnostic potential. Peripheral blood samples were analyzed using flow cytometry. Tim-3 expression and its co-expression with HLA-DR, DP, DQ, CD226, CD39, VNN2, and CD62L were assessed. Tim-3+ monocytes from healthy individuals displayed higher expression of HLA class II, VNN2, CD226, and CD39, but lower CD62L expression. In SLE patients, Tim-3 expression was significantly increased across all monocyte subsets compared with healthy controls, while VNN2 expression was reduced in Tim-3+ monocytes. Upon LPS stimulation, Tim-3+ monocyte subsets produced more TNF-α. The frequency of Tim-3+ monocytes positively correlated with anti-Ro52 and anti-SSA antibodies. ROC curve analysis demonstrated moderate diagnostic performance of Tim-3+ monocytes for SLE, with an area under the curve of 0.7901. Tim-3+ monocytes exhibit aberrant phenotypic and functional activation in SLE and are associated with disease-related autoantibodies. These findings highlight Tim-3+ monocytes as potential contributors to SLE pathogenesis and candidate biomarkers for early disease identification. - Source: PubMed
Gao YimingHan QihuiZheng XiaoyiZong ZhiweiXiong ZiqiZhang ZhonghuiBahabayi AyibaotaLiu Chen - Germline predisposition gene mutations may influence outcomes in patients undergoing hematopoietic stem cell transplantation (HSCT). - Source: PubMed
Publication date: 2026/07/28
Li ZhihuiYang KeyanZhang CaiyanWang XianxuanWang LeiLi JingWen XiaopeiFei QianZhai JiahongZhou YanMing ZongyangSong YanzhiZhao YongqiangWu TongZheng Qinlong