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
Related 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
- 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 - - Source: PubMed
Publication date: 2026/04/09
Chen Andrew A YSchwarzkopf RichardSchrader Kasmintan AChen Luke Y C - We summarise the current knowledge of T-cell immunoglobulin and mucin domain-containing protein 3 (TIM-3) across innate and adaptive immune cells and compile emerging evidence in cardiovascular disease (CVD). - Source: PubMed
Publication date: 2026/04/07
Yousif Laura ISijtema Aukje GChevalier Margot Jde Boer Rudolf AMeijers Wouter C - Primary central nervous system lymphoma (PCNSL) is a rare and aggressive B-cell lymphoma in which early diagnosis remains challenging. Although cerebrospinal fluid (CSF) B-cell-associated factors including soluble interleukin-2 receptor subunit alpha (IL-2RA) are known diagnostic markers, they often reflect neuroinflammation and are insufficient on their own to reliably differentiate PCNSL from neuroimmunological diseases. On the other hand, CSF immune checkpoint molecules reflect neuro-immune regulation and remain incompletely evaluated as biomarkers for PCNSL. We aimed to determine whether CSF immune checkpoint molecules can serve as additional diagnostic and prognostic biomarkers for PCNSL alongside B-cell-associated factors. - Source: PubMed
Publication date: 2026/04/02
Nishii ShotaAkatani RitsuShiroma KyokaTakeda RyosukeTsuji AsatoKatanazaka KimitakaMatoba KentoOtani MayumiKoto ShusukeTanaka KazuhiroNagashima HiroakiSekiguchi KenjiSasayama TakashiChihara Norio