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
- 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 - Persistent antigenic stimulation leads to the dysfunction of CD8 cytotoxic T cells. These "exhausted" T cells exhibit reduced proliferative capacity, impaired effector function, and increased expression of co-inhibitory receptors. Chronic antigen receptor stimulation induces the expression of NFATc1/αA, a short isoform of NFATc1 that promotes T cell survival. The induction of NFATc1/αA is accompanied by a significant decrease in NFATc2 expression. NFATc2 limits the expression of stemness-associated genes, such as , , and It also supports the expression of , , and the T marker gene . Therefore, ablation of NFATc2 mitigates functional exhaustion of CD8 T cells during chronic viral infection and antitumor immunity. Our findings illustrate that NFATc1 promotes the survival of T cells, while NFATc2 promotes the terminal differentiation and dysfunction of exhausted CD8 T cells. The data suggest a non-redundant interplay between NFATc1 and NFATc2, each playing a distinct role in controlling CD8 T-cell exhaustion. These findings open novel avenues to enhance the efficacy of immune checkpoint and CAR T-cell therapies. - Source: PubMed
Publication date: 2026/07/24
Sampere-Birlanga SalvadorKlein-Hessling StefanCampillo Prados MiriamHuang AnfeiWu HaoRosenwald AndreasKastenmüller WolfgangSerfling EdgarVaeth MartinBerberich-Siebelt Friederike - T cell immunoglobulin mucin-3 (TIM-3) plays a critical role in the T cell exhaustion and there have been already many related inhibitory antibodies in clinical trial. However, non-invasive visualization of TIM-3 is lagging in comparison to the development of therapeutic antibodies. This study aims to develop a positron emission tomography/computed tomography (PET/CT) imaging tracer targeting TIM-3 and explore its ability to visualize tumor lesions. - Source: PubMed
Publication date: 2026/07/23
Bao GuangfaZhang JianfangCui YeqianLi DanLu MenglinLu RencaiXv DongdongWu MingkangWang Shaobo - Thyroid cancer (TC) is the most common endocrine malignancy. While papillary thyroid cancer (PTC) generally has a favorable prognosis, anaplastic thyroid cancer (ATC) is rare but highly aggressive, with limited treatment options, highlighting the urgent need for novel therapeutic targets. Macrophages are a major component of the immune infiltrate in TC, and their abundance is associated with poor prognosis. We recently identified upregulation of the immune checkpoint TIM3 (T-cell immunoglobulin and mucin-domain containing protein 3) on M2-like macrophages both in vitro and in ATC xenografts. In addition, we have shown that transforming growth factor β1 (TGFβ1) promotes macrophage polarization toward an M2-like phenotype. However, the role and clinical significance of TGFβ1 in regulating TIM3 expression in TC-associated macrophages remains unclear. We found that TGFβ1 secreted by ATC cells significantly increased HAVCR2 (TIM3) mRNA expression in human monocytes. Analysis of patient samples demonstrated elevated TIM3 expression in both PTC and ATC tissues compared with adenoma and normal thyroid counterparts. Analysis of publicly available single-cell RNA sequencing datasets further showed increased TIM3 expression in T cells from both tumor types. Notably, TIM3 upregulation was also localized to M2-like macrophages within the thyroid tumor microenvironment (TME), and positively correlated with TGFB1/CD163 expression, suggesting the involvement of a TGFβ-TIM3 axis in macrophages in TC. Combined targeting of the TIM3 and PD1 pathway in an immunocompetent mouse model of ATC led to a significant reduction in tumor growth. Together, these findings highlight TIM3 as a promising immunotherapeutic target in TC, with the potential to suppress macrophage-mediated pro-tumor activity while enhancing T-cell-driven anti-tumor immunity within the thyroid TME. © 2026 The Pathological Society of Great Britain and Ireland. This article has been contributed to by U.S. Government employees and their work is in the public domain in the USA. - Source: PubMed
Publication date: 2026/08/05
Jaroszewski AgustinaChoi Yeon-SookHellriegel FlorenciaZhang WeiCarrizo FernandoSong Dong EunLaborie María VictoriaRuggieri MarceloPeretti EmilianoBanus María VictoriaStempin Cinthia CarolinaNicola Juan PabloRodríguez Eva Virginia AcostaDay Chi-PingNeedle GabrielCalifano InésRamacciotti Constanza FernandaIglesias-Bartolome RamiroKim Won GuJeon Min JiFozzatti Laura - Severe pneumonia in children remains a major cause of hospitalization, respiratory failure and infection-related mortality. Increasing evidence indicates that disease severity is shaped not only by pathogen burden but also by the timing, intensity and compartmentalization of the host immune response. CD4+ T cells are central to this process because they coordinate macrophage activation, B-cell help, mucosal defense and immune resolution. In severe disease, however, CD4+ T-cell responses may become depleted, misdirected or constrained by immune-checkpoint pathways. T-cell immunoglobulin and mucin-domain-containing protein 3 (Tim-3/HAVCR2) is a context-dependent immune regulator that may reflect activation, adaptive restraint, regulatory compensation or exhaustion-like dysfunction depending on disease phase and inflammatory milieu. In parallel, cytokines such as interleukin (IL)-6, IL-8, IL-1β and tumor necrosis factor-α amplify neutrophilic inflammation, endothelial activation, vascular leakage and systemic injury. This narrative review synthesizes current evidence on CD4+ T-cell dysfunction, Tim-3 biology and cytokine-mediated immune dysregulation in severe pediatric pneumonia. We propose a checkpointed hyperinflammation framework in which innate cytokine amplification coexists with constrained adaptive immune coordination. However, direct pediatric pneumonia evidence remains limited, and much of the mechanistic interpretation of Tim-3 is extrapolated from adult sepsis, oncologic, chronic infection and autoimmune literature. CD4+Tim-3, soluble Tim-3, and focused cytokine panels therefore can be evaluated in longitudinal pediatric cohorts with pathogen stratification, multi-checkpoint profiling, and blood-airway immune comparison. - Source: PubMed
Publication date: 2026/07/16
Cao FangZhang QiYan Lunan