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anti-tetanus immunoglobulin (Tetglob)

✓ Approved

Bharat Serums and Vaccines Limited · 治疗药物

什么是 anti-tetanus immunoglobulin？

anti-tetanus immunoglobulin 是一种治疗药物，由Bharat Serums and Vaccines Limited研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intramuscular (IM) Injection。

药物档案

商品名Tetglob
公司Bharat Serums and Vaccines Limited
给药途径Injectable (Others), Intramuscular (IM) Injection
状态Approved
来源： ClinicalTrials.gov, Bharat Serums and Vaccines Limited

治疗适应症

anti-tetanus immunoglobulin 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Infections and infestationsTetanus✓ Approved

相关研究文献

PubMedClinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology2026-08-05

Processionary Moth Exposure in Europe: Toxic-Irritant and Immunoglobulin E-Mediated Endotypes, Diagnosis and Management.

Dasari Prasad P, Haas Josefine J, Rohe Wolfgang W, Gloyna Kai K et al.

Processionary moths (Thaumetopoea spp.), particularly the oak processionary moth (Thaumetopoea processionea), are an increasingly relevant cause of allergic and toxic disease in Europe, occurring in the context of reported range expansion, changing environmental conditions and persistent contamination with airborne urticating hairs (setae). Clinical manifestations range from toxic-irritant dermatitis and ocular injury to respiratory symptoms, while a subset of exposed individuals develops genuine IgE-mediated disease, including rhinoconjunctivitis, asthma, and rare cases of anaphylaxis. These presentations reflect two mechanistically distinct endotypes: (i) toxin-driven epithelial penetration by the urticating hairs with neuro-inflammatory activation and (ii) allergen-specific sensitisation to defined molecular components such as Tha p 1 and Tha p 2. Accurate endotype differentiation is clinically relevant, as symptom latency, severity, and risk of systemic progression differ substantially. Diagnostic evaluation relies on exposure history and phenotype recognition, complemented in selected cases and experienced centres by skin testing using research-grade extracts and emerging component-resolved approaches. Basophil activation testing may provide additional mechanistic insights in selected cases. Management comprises prompt decontamination, anti-inflammatory therapy, urgent ophthalmologic assessment when eye involvement is suspected, and guideline-based management of anaphylaxis. The environmental persistence of setae and recurrent seasonal exposure highlight the need for improved surveillance, validated molecular diagnostics, and translational research defining immune mechanisms and biomarkers.

PMID 42554243
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PubMedHuman gene therapy2026-08-05

Suppression of AAV-Delivered Transgene Expression Using Artificial MicroRNAs Delivered by an Alternative AAV Serotype.

de Mulder Rougvie Miguel M, Kebret Mara R MR, Wu Youjun Y, Stiles Katie M KM et al.

Adeno-associated virus (AAV) gene transfer vectors mediate long-term expression in nondividing cells, an advantage for treating chronic disorders. However, current platforms lack a way to selectively shut down transgene expression if adverse effects arise. To create an "off switch," we hypothesized that incorporating unique artificial microRNA (amiRNA) target sequences into an AAV expression cassette would allow subsequent suppression of transgene expression using a second AAV vector encoding the cognate amiRNA. We introduced 22-nt sequences absent from human and mouse transcriptomes into the 3' untranslated region (UTR) of a therapeutic AAV cassette. To identify optimal amiRNAs, two tandem copies of each amiRNA were cloned into the 3'UTR of an mCherry reporter gene. In vitro assessment of six amiRNA/target pairs using a dual luciferase assay identified four amiRNAs that efficiently suppressed reporter expression. Cells cotransfected with target site 3 (TS3) and amiRNA-T3B showed the greatest reduction in luciferase activity (80%, p < 0.0001) and were selected for further study. The "off-switch" system was then evaluated using an AAV5 therapeutic vector expressing a recombinant humanized anti-IgE monoclonal antibody (AAV5-TBG-anti-IgE-TS3), designed for long-term suppression of allergen-induced reactions. Co-transfection of HEK293T cells with anti-IgE-TS3 and amiRNA-T3B significantly reduced anti-IgE mRNA and protein levels relative to a control amiRNA (p < 0.0001). In vivo testing in Balb/c mice (n = 5) involved intravenous administration of AAV5-anti-IgE-TS3 (3.2 × 1010 gc), followed 4 weeks later by an AAVrh.10 amiRNA vector (AAVrh.10-TBG-amiRNA-T3B; 1 × 1011 gc). Control mice receiving only the therapeutic vector expressed 18.4 ± 13.8 µg/mL serum anti-IgE at 10 weeks. In contrast, mice receiving the amiRNA "off" vector showed marked suppression of anti-IgE (0.3 ± 0.15 µg/mL, p < 0.0001). These findings provide proof-of-concept that AAV-delivered amiRNAs can selectively switch off transgene expression, offering a strategy to improve the safety of AAV-mediated gene therapies.

PMID 42552862
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PubMedFrontiers in endocrinology2026-08-05

Zinc, type 2 diabetes, diabetic kidney disease: focus on hypoxia.

Lebedeva Svetlana A SA, Mikhailova Ekaterina M EM, Materenchuk Maria Yu MY, Kurkin Denis V DV et al.

The incidence of type 2 diabetes mellitus is approaching pandemic levels, posing a major global healthcare problem. Diabetic kidney disease (DKD) is the main cause of the chronic kidney disease. Hyperglycemia-dependent renal hypoxia drives the onset and progression of DKD. The adaptive cellular response to hypoxia depends on the zinc signalling, which promotes expression of the hypoxia-inducible factor-1α (HIF-1α). Zinc is further relevant for anti-inflammatory, antioxidant, anti-apoptotic, and anti-fibrotic signalling pathways with nephroprotective effects in DKD. In this review, we focus on the role of zinc homeostasis in the development of diabetes and DKD, with particular emphasis on hypoxia as the central trigger of DKD. We also discuss the role of the zinc signaling in the cellular and systemic carbohydrate metabolism in the context of diabetes and DKD.

PMID 42553224
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PubMedLab on a chip2026-08-05

Differential modulation of exhausted Th1 cell migration by immune checkpoint blockade: insights from 3D microfluidic and in vivo PDX platforms.

Horzum Utku U, Yanik Hamdullah H, Tavukcuoglu Ece E, Taskiran Ekim Zihni EZ et al.

Effective anti-tumor immunity is critically dependent on the functional capacity and robust infiltration of type-1 helper T (Th1) cells into the tumor microenvironment (TME). However, persistent antigenic stimulation leads to T cell exhaustion, determining the efficacy of immunotherapy approaches such as immune checkpoint inhibitors (ICIs). A key barrier to successful immunotherapy therapy remains the impaired motility and infiltration of exhausted T cells. To address this, we investigated the dual impact of anti-PD-1 and anti-CTLA-4 blockade on the migratory efficacy of ex vivo generated exhausted Th1 (Th1-Ex) cells. Recognizing the limitations of 2D culture, we utilized a 3D microfluidic (lab-on-a-chip) platform to simulate the TME's complex physical and chemical constraints, alongside in vivo patient-derived xenograft (PDX) models. While ICI treatment did not alter static adhesion, it distinctly modulated focal adhesion dynamics. Critically, in the highly relevant 3D microfluidic environment, ICI-treated Th1-Ex cells exhibited significantly enhanced motility and directional persistence compared to untreated cells. Mechanistically, anti-PD-1/CTLA-4 treatment activated signalling pathways associated with both amoeboid and mesenchymal-like migration, but functional inhibition identified RAC1-dependent mesenchymal-like migration as the predominant contributor to the enhanced migratory response. These results were strongly corroborated in vivo, where the anti-PD-1/CTLA-4 combination conferred remarkable and selective tumor and lymph node infiltration capacity to the adoptively transferred Th1-Ex cells. Collectively, our findings highlight a dual role for ICIs on restoring Th1 cell functionality and actively promoting tumor-directed migration by altering adhesion-migration pathways, offering novel mechanistic insights for optimizing immunotherapies in solid tumors.

PMID 42552843
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PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-08-05

Redirecting Monocyte Differentiation With Engineered Extracellular Vesicles for Glioma Immunotherapy.

Pan Yuanwei Y, Liu Xuan X, Meng Qian-Fang QF, Cao Lei L et al.

During glioma progression, monocytes abundantly infiltrate but primarily differentiate into immunosuppressive macrophages to promote tumor growth. Redirecting monocyte differentiation offers a compelling yet underexplored therapeutic opportunity. In this work, we found M1-polarized macrophage-derived extracellular vesicles (M1-EVs) efficiently induced monocytes to differentiate into anti-tumor macrophages via tumor necrosis factor alpha (TNF-α)-mediated signaling. Despite promising, the therapeutic efficacy of M1-EVs was constrained by insufficient glioma accumulation and CD47-mediated phagocytic inhibition. To address this challenge, we further engineered M1-EVs with dual-targeting specificity by genetically incorporating a tumor-directed chimeric antigen receptor (CAR) against IL13Rα2 or EGFRvIII together with CD47-blocking SIRPα variants. The resulting dual-targeting EVs (M1-CS-EVs) exhibited enhanced blood-brain barrier (BBB) penetration and glioma accumulation while locally disrupting CD47-SIRPα interactions. In three orthotopic glioma models, M1-CS-EVs elicited a potent anti-tumor immune response and enhanced tumor phagocytosis, significantly suppressing tumor growth while prolonging animal survival. Our findings establish a platform technology for directing monocyte differentiation toward anti-tumor phenotypes, offering a broadly applicable strategy for glioma treatment.

PMID 42554595
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PubMedArchive of clinical cases2026-08-05

ESA-induced pure red cell aplasia presenting as a precipitous hemoglobin drop in end-stage renal disease.

Mui James Seng Koon JSK

Anemia is a nearly universal complication of chronic kidney disease (CKD). While erythropoiesis-stimulating agents (ESAs) are the standard of care, they rarely induce acquired pure red cell aplasia (PRCA) via neutralizing anti-erythropoietin (anti-EPO) antibodies. Diagnosis is often delayed as clinical focus frequently shifts toward more common causes of acute anemia, such as hemorrhage. An 88-year-old male on maintenance hemodialysis presented with a precipitous hemoglobin drop to 6.8 g/dL. Investigation revealed replete hematinics but profound reticulocytopenia. After excluding occult gastrointestinal bleeding, hemolysis, and nutritional deficiencies, a bone marrow biopsy demonstrated isolated erythroid aplasia with preserved myeloid and megakaryocytic lineages, leading to a diagnosis of PRCA. Anti-EPO antibody testing was not performed, which limits definitive etiological confirmation. Due to the high risk of immunosuppression in an elderly patient and the limited accessibility of hypoxia-inducible factor-prolyl hydroxylase inhibitors (HIF-PHIs), management was restricted to ESA cessation and supportive transfusions. This case highlights the diagnostic approach for severe anemia and the significance of profound reticulocytopenia in PRCA. The definitive hallmark remains the detection of circulating anti-EPO antibodies paired with a bone marrow study demonstrating near-total depletion of erythroid precursors, but preserved myeloid and megakaryocyte lineages. Management includes the permanent cessation of ESAs, immunosuppression to reduce circulating antibodies, and supportive blood transfusions. In chronic hemodialysis patients, early recognition of iatrogenic PRCA is essential to prevent the continued administration of potentially harmful ESAs and to facilitate a transition toward alternative therapies, such as HIF-PHIs.

PMID 42553667
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