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
- Neurodegenerative diseases are increasingly recognized as disorders shaped not only by intrinsic neuronal vulnerability, but also by chronic neuroinflammation mediated by maladaptive neuroimmune signaling. Granzymes, a family of serine proteases classically studied for their cytotoxic roles in anti-viral and anti-tumor immunity, are emerging as important mediators of central nervous system (CNS) pathology. In addition to their canonical intracellular functions, granzymes can act extracellularly to cleave the extracellular matrix (ECM), activate cell-surface receptors, disrupt epithelial barrier function, amplify inflammatory cascades, and alter glial and neuronal responses to injury. In this review, we synthesize current knowledge on the roles of Granzyme A (GzmA), Granzyme B (GzmB), Granzyme H (GzmH), and Granzyme K (GzmK) in neurodegeneration and neuroinflammation across diverse CNS disease and injury contexts, such as Alzheimer's disease (AD), multiple sclerosis (MS), stroke, spinal cord injury (SCI), and age-related macular degeneration (AMD). GzmB is the most extensively characterized, with evidence supporting both intracellular neurotoxicity and extracellular pathogenic functions mediated through protease-activated receptor signaling, ECM cleavage, outer blood-retina barrier disruption, angiogenesis, fibrosis, and chronic inflammation. GzmA is implicated in tau proteolysis and structural destabilization of neurons and astrocytes, while GzmK has emerged as a context-dependent regulator of neuroinflammation through PAR-1 activation, microglial modulation, and complement cascade activation. GzmH remains the least understood but may contribute to nerve injury through mechanisms that are only beginning to be defined. We also discuss endogenous and pharmacological granzyme inhibition, highlighting the therapeutic promise of selective extracellular granzyme targeting, particularly for GzmB, while emphasizing the current lack of selective inhibitors for GzmA, GzmK, and GzmH. Collectively, these findings position granzymes as underappreciated neuroimmune effectors and potential therapeutic targets in neurodegenerative diseases and CNS injury. - Source: PubMed
Publication date: 2026/08/18
Yoo Hyung-SukYu PhilipZhou CeresHosseini AmirGranville David JMatsubara Joanne A - Visceral leishmaniasis (VL), a parasitic disease caused by Leishmania donovani, requires a robust CD4 T-cells response to control parasite replication by interferon-gamma (IFN-γ) production and activation of macrophages. However, in VL patients, the anti-parasitic CD4 T-cell responses are ineffective for reasons that are still unclear. Our recent study reporting a transcriptional signature of CD4 T-cell isolated from the peripheral blood of active VL patients showed enhanced expression of genes related to cytotoxicity. This study investigates the cytotoxic potential of CD4 T-cells in VL patients, focusing on the expression of the key cytotoxic molecules granzyme B (GZMB), granulysin (GNLY), perforin (PRF), natural killer cell granule protein 7 (NKG7) and the degranulation capacity of CD4 T-cells during infection. We observed significant upregulation of these cytotoxic markers in CD4⁺ T-cells from VL patients, particularly prior to anti-parasitic drug treatment (D0), suggesting activation of these cells. However, the degranulation capacity, as indicated by CD107a expression, was comparable between VL patients and endemic controls (ECs), suggesting potential functional impairment in the cytotoxic response. Yet, antigen-specific GZMB secretion in whole blood cultures and intracellular GZMB production in CD4 T-cell subsets (notably Th1, Th9 and Th17/22 cells) were enhanced in VL patients, indicating a robust antigen-specific response, though this did not translate into effective parasite control. These findings highlight a paradox whereby CD4 T-cells from VL patients have heightened production of cytotoxic molecules, but lack translocation of CD107a to the cell surface, which is associated with an inability to eliminate parasites. This study provides new insights into the immune dysfunction in VL, highlighting a potential role for the cytotoxic phenotype that develops in parasite-specific CD4 T-cells. Targeting these pathways may offer novel therapeutic strategies to enhance immune responses and improve clinical outcomes in VL. - Source: PubMed
Chauhan Shashi BhushanSingh Siddharth SankarSingh BhawanaKumar ShashiTiwari RahulGautam VibhavRivera FabianNylen SusanneEngwerda ChristianSundar ShyamKumar Rajiv - Tumor infiltrating CD8 T cells (TILs) progress to a state of terminal exhaustion (Ttex) which have impaired functionality and are nonrenewable. However their precursors (Tpex) are renewable and can generate efficient effector cells. We started from the observation that melanoma patients undergoing therapy with checkpoint inhibitors show increased survival when their T cells have low mRNA. In line with this, ablation of in CD8 TILs conferred a superior anti-tumor response in murine melanoma and ovarian cancer models. KO TILs failed to progress to the Ttex state and retained elevated stemness. Bcl11b exerted its role by repressing expression of essential transcription factors (TF) controlling stemness, and conversely by promoting expression of exhaustion-associated TFs and inhibitory receptor genes, through complex epigenetic control. In addition, KO CD8 T cells showed increased Ag-specific cytolytic activity and elevated Gzmb and Prf1 proteins, but no increase in their mRNAs, however presented higher expression of genes with role in translation. Furthermore, CRISPR-CAS9-mediated deletion of BCL11B in human TILs from a patient with poor response to adoptive cell therapy with autologous TILs, improved their cytolytic activity and promoted expression of the stemness-associated TF TCF1, underlying its potential therapeutic use. - Source: PubMed
Publication date: 2026/08/07
Silvane LeonardoZelenka TomasTalada Divya PCismasiu Valeriu BIslam ShamimaSingh Raghwendra PNgove ZefaniasChakraborty SayanHall MacLean SBlauvelt Jamie LEksioglu ErikaManrique Soraya ZorroJohnson Joseph OObermayer Alyssa NAlfaro AlexHuang WenSarnaik AmodTarhini Ahmad AMullinax John EGeorge ErinHwu PatrickDavila EduardoConejo-Garcia Jose RBryceson Yenan TChen Dung-TsaShaw Timothy IPilon-Thomas ShariAvram Dorina - Breast cancer (BC) is a disease that occurs relatively frequently, and its prognosis and treatment outcomes are not optimal at present. Identifying novel BC biomarkers and therapeutic targets is key. DEAH-box helicase 15 (DHX15) is an RNA helicase that exhibits enhanced activity and is closely associated with tumorigenic potential. Alternative splicing is widely dysregulated in BC. However, the biological function of DHX15 in BC, in addition to its underlying molecular mechanisms, remain unclear. DHX15, a key RNA helicase involved in splicing regulation, was therefore selected to explore whether it modulates the malignant progression of BC. The present study therefore analyzed the DHX15 expression profile in BC using the Tumor Immune Estimation Resource database. Kaplan-Meier plotter database was utilized to investigate the prognostic value of DHX15 in BC. The Cancer Genome Atlas-BRCA database was utilized to investigate the association between DHX15 and immune infiltration, as well as the expression of immune biomarkers, within the tumor microenvironment. The potential biological functions of DHX15 in BC were also investigated using Gene Ontology (GO) enrichment analysis, Kyoto encyclopedia of genes and genomes pathway analysis (KEGG) and single-cell functional analysis. GO and KEGG enrichment analyses were performed via the GSEA module embedded in the LinkedOmics database. Single-cell functional analysis was performed using the Human Proteome Atlas database and the CancerSEA database. Concurrently, the expression and function of DHX15 in BC was validated. MDA-MB-231 cells were transfected with a DHX15 knockdown plasmid and MCF-7 cells with an overexpression plasmid, and Transwell assays, plate cloning and scratch assays were performed on the established cell lines. The present findings revealed that the DHX15 expression levels in BC were notably higher compared with those in normal tissues. Furthermore, the expression of DHX15 was associated with immune checkpoints (such as PDCD1, LAG3 and GZMB) and immune cell infiltration (such as T helper cells and central memory T cells) in BC, as determined by single-sample Gene Set Enrichment Analysis and CIBERSORT analyses. experiments suggested that inhibiting DHX15 notably suppressed the migration, invasion and proliferation of MDA-MB-231 cells. Collectively, these findings suggest that the high expression of DHX15 in BC is associated with worse prognosis and immune cell infiltration, potentially by functionally promoting tumor cell proliferation, migration and invasion. - Source: PubMed
Publication date: 2026/08/05
Li FanYue QinLi Jing - Immune escape is a hallmark of cancers, which affects the efficacy of immunotherapy. Herein, this study analyzed the significance of GATA1/FGL1 in the immune escape of cervical squamous cell carcinoma (CESC) to deepen the understanding of immune escape-associated molecular mechanisms. In silico analysis predicted the correlations of FGL1 with CESC prognosis and CD8 T cell infiltration as well as the relation between FGL1 and GATA1. After FGL1 and/or GATA1 gain- and loss-of-function, CC cells were co-cultured with CD8 T cells. The sensitivity of CC cells to CD8 T cells was assessed, as well as the secretion of perforin, GzmB, IFN-γ, and TNF-α. Also, CD8 T cell proliferation and apoptosis were measured. The binding of GATA1 to the FGL1 promoter was validated through luciferase and ChIP assays. GATA1-knockdown U14 cells were transplanted into immunocompetent C57BL/6 mice in combination with or without CD8α mAb to ascertain the impacts of GATA1 on tumor growth and immune escape in CESC in vivo. Knockdown of either FGL1 or GATA1 markedly enhanced the sensitivity of CC cells to CD8 T cell‑mediated cytotoxicity and increased the secretion of perforin, GzmB, IFN‑γ, and TNF‑α. It also promoted CD8 T cell proliferation while reducing their apoptosis. These effects of GATA1 knockdown were partially negated by FGL1. In vivo, GATA1 knockdown prominently diminished the tumor growth and increased the infiltration and cytotoxic effects of CD8 T cells. Collectively, GATA1 knockdown facilitates CD8 T cell responses and suppresses immune escape in CESC by downregulating FGL1. - Source: PubMed
Publication date: 2026/08/13
Zhou JuanLiu FangGao TingtingYang Ying