TIMD3 _ HAVCR2 Antibody
- Known as:
- TIMD3 _ HAVCR2 Antibody
- Catalog number:
- 10390-RP01
- Product Quantity:
- 200
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- TIMD3 _ HAVCR2 Antibody
Related genes to: TIMD3 _ 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 _ HAVCR2 Antibody
Related articles to: TIMD3 _ HAVCR2 Antibody
- Colorectal cancer (CRC) remains the leading cause of cancer-related mortality worldwide and necessitates the development of novel therapeutic strategies. The tumor immune microenvironment (TME) critically influences disease progression and the response to immune checkpoint inhibitors (ICIs). Tumor-infiltrating lymphocytes (TILs) are key components of the TME with established prognostic and predictive significance. Nevertheless, detailed TIL characterization using flow cytometry has not been fully investigated in CRC. - Source: PubMed
Matoba DaijiroSaito TakuroNoda TakehiroUemura MamoruUeyama AzumiWada HisashiDoki YuichiroEguchi Hidetoshi - Survival outcomes for pediatric Burkitt lymphoma (BL) substantially vary depending on geography (50-90%), which also serves as a proxy for the prevalence of Epstein-Barr virus (EBV) within the tumors. Although BL is considered an immunologically "cold" tumor with few tumor-infiltrating lymphocytes (TILs), their functional status has not been fully evaluated, especially for EBV-positive disease. Here, we characterize the exhaustion and activation profiles of T cells in the tumor microenvironment (TME) of EBV-positive BL using orthogonal methods, single-cell gene expression analysis, spectral flow cytometry, and immuno-histochemistry staining (IHC). We found that CD8+ TILs displayed a mosaic of immune inhibitory gene expression encoding, PD1, TIGIT, LAG3 and HAVCR2/TIM3. IHC validated the expression of PD1 and TIGIT on CD8+ TILs, as well as their respective ligands, PDL-1, PVR, and Nectin-2 on malignant B cells. Despite exhaustion-associated signatures, CD8+ TILs retain cytotoxic potential, expressing granules (i.e. Granzyme A, Perforin) and cytokines (i.e. IFNγ) and demonstrate an increased uptake of metabolites such as glucose, arginine, and methionine. In peripheral blood, pediatric BL patients exhibited a significantly higher abundance of PD1+TIGIT+ CD8+ T cells compared to healthy children. Notably, these circulating T cells from BL patients express significantly lower levels of TOX, suggesting they are not irreversibly dysfunctional. Together, our results indicate that CD8+ T cells both in the TME and in circulation of children with BL are not terminally exhausted but remain poised for functional re-invigoration. These findings support the potential integration of immune checkpoint inhibitors into combination chemotherapeutic regimens to improve outcomes for these children. - Source: PubMed
Publication date: 2026/04/19
Forconi Catherine SOduor Cliff ISaikumar Priya LRacenet Zachary JFujimori GavinM'Bana ViriatoMatta AngelaMelo JeniLaderach FabienneMaina Titus KOtieno Juliana AChepsidor DanKibor KibetNjuguna FestusVik TerryKinyua Ann WMunz ChristianBailey Jeffrey AMoormann Ann M - Pregnancy is characterized by significant changes in peripheral immunity. Total CD3+ T cells decrease across pregnancy while Forkhead Box P3+ T-regulatory cells (FoxP3+Tregs) peak in mid-pregnancy, the latter of which are key to healthy outcomes. However, less is known regarding distinct memory populations of FoxP3+ Tregs and their phenotypic changes across pregnancy. - Source: PubMed
Mulugeta NolawitPeters M QuinnTobey CaraWong JiaSpray Abigail L PArmistead BlairJiang YonghouKatz RonitShree RajVojtech LuciaHarrington Whitney E - Chimeric antigen receptor (CAR) T-cell therapies have transformed the treatment of B-cell malignancies, yet challenges including manufacturing delays, T-cell exhaustion, and limited persistence impede broader clinical success. Here, we report the single day production of non-activated CAR T-cells engineered to secrete interleukin-18 (IL-18), a pro-inflammatory cytokine that enhances T-cell function. These non-activated CART-IL18 cells exhibit robust anti-tumor efficacy across xenograft models of lymphoma, leukemia, and pancreatic cancer. IL-18 expression enhances the functional advantages of naïve-like non-activated CAR T-cells, resulting in improved persistence, metabolic fitness, and resistance to exhaustion. Single-cell transcriptomic analysis revealed upregulation of IL7R, KLF2, and MCL1, alongside suppression of inhibitory checkpoint genes such as PDCD1, TOX, and HAVCR2. Metabolomic profiling demonstrated enhanced mitochondrial bioenergetics, with increased spare respiratory capacity and accumulation of α-ketoglutarate, malate, and spermine. Functional in vitro and in vivo profiling demonstrated enhanced per-cell cytotoxicity and in vivo durability. We complemented these studies with single-cell transcriptomic and metabolomic analyses to define CAR T-cell biological states beyond what is captured by xenograft tumor clearance. This IL-18-enhanced, activation-free CAR T product offers a clinically actionable platform with the potential to reduce vein-to-vein time while improving product potency and persistence, providing a rationale for clinical testing in patients with tumors refractory to standard CAR T. - Source: PubMed
Publication date: 2026/04/16
Durgin Joseph SSeo Shin HKazmi ShadabValentić BakirLeff ChloeMarkovska MartinaJin XiaolingShen FengBerjis AbdullaMukherjee NandanaSannecy AshwinPlesa GabrielaGabunia KhatunaScholler JohnGill Saar IO'Connor Roddy SJune Carl HGhassemi Saba - This study aimed to examine the regulatory effects of moxibustion on macrophage polarization and migration in a rat model of rheumatoid arthritis, as well as the role of T cell immunoglobulin and mucin domain-containing protein 3 (TIM-3) in this process. On day 0 of the experiment, Sprague-Dawley (SD) rats were divided into five groups. Complete Freund's adjuvant (CFA) was injected into the hind footpads to establish the rheumatoid arthritis model. Additionally, lentivirus-mediated Havcr2 RNA interference (LV-Havcr2-RNAi) was injected into the hind footpads to inhibit TIM-3 expression. Starting on day 7, rats underwent moxibustion treatment in cycles comprising six days of treatment and one day of rest, for a total of three complete cycles. After completion of moxibustion therapy, the inflammatory status was assessed through histological analysis and measurement of paw thickness. Phenotypic markers of M1 and M2 macrophages were assessed by enzyme-linked immunosorbent assay (ELISA) and immunofluorescence. TIM-3 expression was detected via quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. Furthermore, peritoneal exudate macrophages (PEMs) were isolated from additional SD rats, and macrophage migration was examined using a Transwell assay. The study found that after CFA injection, rats exhibited significant paw redness and swelling, along with an imbalance in macrophage phenotype expression. Additionally, Transwell migration assays revealed that CFA-induced model rats showed increased macrophage migration relative to control specimens. However, moxibustion treatment attenuated these changes. Results also demonstrated that moxibustion increased TIM-3 expression, and after lentiviral intervention, TIM-3 levels were markedly reduced, leading to exacerbation of inflammatory manifestations and macrophage imbalance. These results indicate that TIM-3 serves as a key mediator in moxibustion regulation of macrophage polarization and migration. - Source: PubMed
Publication date: 2026/03/27
Nie JingweiWang SiyuXu YimeiCui LuHuang JunHuang ZhicanZhou Haiyan