Granzyme B _ GZMB Antibody
- Known as:
- Granzyme B _ GZMB Antibody
- Catalog number:
- 10345-RP03
- Product Quantity:
- 200
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- Granzyme _ GZMB Antibody
Related genes to: Granzyme B _ GZMB Antibody
- Gene:
- GZMB NIH gene
- Name:
- granzyme B
- Previous symbol:
- CTLA1, CSPB
- Synonyms:
- CCPI, CGL-1, CSP-B, CGL1, CTSGL1, HLP, SECT
- Chromosome:
- 14q12
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-12
- Date modifiied:
- 2016-10-05
Related products to: Granzyme B _ GZMB Antibody
Related articles to: Granzyme B _ GZMB Antibody
- Abnormal lipid accumulation in the tumor microenvironment (TME) promotes lipid peroxidation in tumor-infiltrating CD8T cells (CD8TILs), driving their dysfunction and impairing antitumor immunity in ovarian cancer (OC). To elucidate the underlying immunosuppressive mechanisms, we integrated clinical specimens, mouse models, and in-vitro validation. Notably, CD8TILs from OC patients exhibited pronounced lipid peroxidation signatures. Elevated oxidized low-density lipoprotein (oxLDL) levels were detected in ovarian tumor interstitial fluid (TIF), tumor mass-derived supernatants, and tissue sections, correlating with accelerated peroxidation phenotype in CD8TILs. Bulk RNA sequencing and experimental validation revealed LOX-1 as the dominant oxLDL receptor in CD8TILs, where its expression was positively correlated with peroxidation levels and negatively linked to PRF1, GZMB, and IFNG expression. In ID8 mouse OC models, LOX-1 expression and lipid peroxidation in CD8TILs increased with tumor progression, and LOX-1-neutralizing antibody treatment partially reversed these changes and restored T-cell function. In vitro, LOX-1 blockade reduced oxLDL-induced lipid peroxidation, restored IFN-γ and GZMB production, and downregulated PD-1 expression, whereas LOX-1 overexpression exerted the opposite effects. Notably, the antioxidants, not ferroptosis inhibitors, restored CD8T cell effector function by suppressing peroxidation. Mechanistically, oxLDL/LOX-1 signaling activated the transcription factor ELF3, which subsequently bound to the PDCD1 promoter to drive PD-1 expression. Together, this study demonstrates that in CD8TILs, LOX-1-mediated uptake of oxLDL induced lipid peroxidation via oxidative stress and establish the oxLDL/LOX-1 axis as a pivotal pathway through which lipid peroxidation impairs CD8TILs function in OC. Targeting LOX-1 or employing antioxidants restored the antitumor capacity of CD8TILs, providing a mechanistic basis for metabolically modulating T cell-based cancer immunotherapy. - Source: PubMed
Publication date: 2026/07/20
Wang TingYan LinaHuang XiZhou LingfeiMao YepengLiu ShunaFu XinLi JinghangTao ZiqiLiu ZhijieZhang YueluSong TingTingJin YuexinziWang Fang - CD8 T cells are critical players in immune responses against pathogens. Interleukin-21 (IL-21) is predominantly produced by CD4 T cells and exerts multifaceted effects on CD8 T cell regulation and function. Using -reporter and -fate mapping mice, we report that a subpopulation of activated CD8 T cells also produces IL-21 in the context of lymphocytic choriomeningitis virus (LCMV) infection. During the early effector phase of both acute and chronic infections, IL-21-expressing CD8 T cells exhibit substantial proliferative and cytotoxic capacities, with higher levels of interferon-γ (IFN-γ) and granzyme B (GZMB) compared with IL-21 counterparts. Moreover, CD8 T cell-derived IL-21 played a critical protective role in chronic, but not acute, infection. IL-21 expression in CD8 T cells appeared to be largely restricted to exhausted progenitor T cells during the exhaustion phase of chronic infection. These findings identify IL-21-expressing CD8 T cells as pivotal players in the control of chronic infection. - Source: PubMed
Publication date: 2026/07/31
Zhao ZixuanFeng HanZhao XiaohongXie BowenXie TianSun QinliChen YongzhenWei KunPan BiruiWei PengZhong XuanYuan LeiBai XueWang XiaohuDong Chen - Immune checkpoint therapies have transformed clinical practice; however, reliable biomarkers to predict response remain limited. Tumor mutational burden (TMB) has emerged as an important biomarker because it is thought to reflect neoantigen load, yet its predictive utility has been inconsistent. This limitation may partly arise because TMB primarily captures tumor-intrinsic immunogenicity, which is heterogeneous and does not fully reflect the state of antitumor immunity. To identify transcriptomic surrogates that capture both high mutational burden and antitumor immune activation, we investigated whether mRNA expression of mutagenic APOBEC3 family members could serve as surrogates for high TMB and T cell-rich tumors. Using a pan-cancer computational framework, we evaluated the association of four APOBEC3 genes with mutational burden, neoantigen load, immune infiltration, and immune checkpoint blockade response. Among , and , emerged as the strongest and most consistent marker of a TMBCD8 and NeoantigenCD8 tumor phenotypes. Single-cell analyses further demonstrated that is enriched in both malignant cells and T cells compared with other family members, with -positive CD8 T cells exhibiting elevated activation markers including GZMB and IFNG. Importantly, retrospective analyses of 50 immune checkpoint blockade cohorts showed that had the most consistent association among family members with treatment response and clinical outcomes. Together, these findings identify as a candidate transcriptomic marker of a TMB-associated, T cell-inflamed tumor state linked to immune-checkpoint blockade benefit, warranting further prospective validation. - Source: PubMed
Publication date: 2026/07/13
Butler Kelly EYesudhas DhanushaLone BilalBanday A Rouf - Interstitial lung disease (ILD) is a common but serious extra-articular manifestation of rheumatoid arthritis (RA). RA-associated ILD (RA-ILD), which often presents with the usual interstitial pneumonia (UIP) pattern, can resemble idiopathic pulmonary fibrosis (IPF), though the treatment and progression of these two conditions differ. However, the immunologic and molecular mechanisms associated with RA-ILD and IPF development have not been well elucidated at the single-cell level. - Source: PubMed
Publication date: 2026/07/28
Kim DongjunLee HyunKim Sang-HeonEun YeongheeKim Hyun JeKim Bo-Guen - Zygnematophytes emerged as the unexpected closest algal relatives of land plants despite their simple body plans, raising questions about the morphogenetic toolkit present in the last common ancestor of land plants and algae. Genomic analyses have revealed that zygnematophytes are cellular giants, sharing homologous frameworks for several phytohormones, secondary metabolites, and key morphogenetic and transcriptional regulatory processes. Zygnematophytes fall into five orders, each of which has chartered its own evolutionary path. Here, we have sequenced a contiguous genome of Spirogyra pratensis, the eponymous representative of Spirogyrales and a classical model system for evolutionary cell biology in the green lineage. Building on this genome, we transcriptionally profiled the tractable life cycle of Spirogyra and its responses to a bifactorial gradient of light and temperature. Our data highlight the activation of quiescence and homeostatic programs. Yet what stands out most in Spirogyra is its spiral chloroplast-undulating intracellularly and abscising during mixed phragmoplast formation and furrowing. Leveraging the genome in tandem with co-expression network analyses, we describe the molecular underpinnings of the unique cytokinetic processes that govern both cell and plastid division. We find that Spirogyra deploys a molecular program characteristic of Phragmoplastophyta, yet lacks the deeply conserved plastid division machinery found in other archaeplastid plastids. - Source: PubMed
Publication date: 2026/07/28
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