Ask about this productRelated genes to: TLR4 antibody
- Gene:
- TLR4 NIH gene
- Name:
- toll like receptor 4
- Previous symbol:
- -
- Synonyms:
- hToll, CD284, TLR-4, ARMD10
- Chromosome:
- 9q33.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-25
- Date modifiied:
- 2016-01-21
Related products to: TLR4 antibody
Related articles to: TLR4 antibody
- Immunotherapy has emerged as a new pillar of cancer therapeutics that utilizes the patient's own immune system to target tumor cells, a particular advantage in the context of hard-to-treat cancers. Virus-based immunotherapies have shown great potential as cancer treatments, including oncolytic viruses, viral vectors and virus-like particles. Here, we discuss the development, applications, challenges, and future opportunities of cowpea mosaic virus (CPMV) as a plant virus-based candidate for intratumoral immunotherapy, focusing on the treatment of aggressive, metastatic and refractory solid tumors. Evidence of antitumor efficacy has been gathered from mouse tumor models and veterinary clinical trials involving canine cancer patients. CPMV is promising as a monotherapy and as part of combination therapies, including chemotherapy, radiation, checkpoint inhibitors, and cytokine therapies. The putative mechanism of action is described, highlighting key features such as the capsid proteins and RNA acting as Toll-like receptor (TLR) agonists for TLR-2, TLR-4 and TLR-7, as well as the presentation of unique epitopes that prime a Th-1 balanced immune response. The nanoparticle structure of CPMV enhances efficacy by exerting multivalency and avidity effects. The biodistribution, toxicity, and agronomical safety profile of CPMV is also described, especially in relation to tumor retention, hematologic toxicity, allergenicity and adverse events, and viral shedding. This body of work provides a thorough exploration of a novel cancer immunotherapy in development for more than 10 years, positioning CPMV as a versatile intratumoral platform with promise for hard-to-treat cancers. - Source: PubMed
Publication date: 2026/05/11
Pottenger Ayumi EOmole Anthony OSteinmetz Nicole F - Enteropathogenic Escherichia coli (EPEC) infection remains a major cause of intestinal barrier dysfunction and diarrhea, necessitating the development of novel non-antibiotic therapies. While Pediococcus pentosaceus (P. pentosaceus) exhibits probiotic potential, the specific role of its postbiotic components, particularly extracellular vesicles (EVs), in host-pathogen interactions remains obscure. In this study, we systematically evaluated the protective efficacy and underlying mechanisms of P. pentosaceus DF29 (DF29) and its derived EVs (PpEVs) against EPEC-induced enteritis. Characterization revealed that PpEVs isolated via ultracentrifugation exhibited a typical vesicular morphology, high purity, and robust stability under simulated gastrointestinal conditions. In vitro, PpEVs were efficiently internalized by macrophages and significantly blunted EPEC-induced pro-inflammatory responses. In vivo, oral administration of PpEVs recapitulated the protective effects of live DF29, including alleviating body weight loss, reducing disease activity index, and restoring histological integrity. Crucially, PpEVs reinforced the intestinal barrier by upregulating tight junction proteins, mitigating oxidative stress, and rebalancing the dysbiotic gut microbiota. Mechanistically, we demonstrated that PpEVs exerted their anti-inflammatory effects by inhibiting the TLR4/MyD88/NF-κB signaling axis, thereby shifting macrophage polarization from an M1 proinflammatory to an M2 anti-inflammatory phenotype and rectifying the Th1/Th2 and Th17/Treg imbalances. Collectively, our findings suggest that PpEVs represent a potential intervention strategy to preserve intestinal homeostasis and counteract EPEC-associated inflammation. - Source: PubMed
Publication date: 2026/05/12
Pan TianxuWang XuetingWang YaZhao DongyuLi HongyeLi HechunLi SongyangGuo TiankuiWang NanHuang HaibinYu ShuyuanGuan JiayaoLiu MingxiaoShi ChunweiWang ChunfengLi MinghanYang Guilian - One-lung ventilation (OLV), essential in thoracic surgery, frequently induces acute lung injury characterized by inflammation and impaired oxygenation. Penehyclidine hydrochloride (PHC) has demonstrated organ-protective potential, but its efficacy against OLV-induced injury and the underlying mechanisms, particularly concerning macrophage polarization and metabolic reprogramming, remain poorly defined. - Source: PubMed
Publication date: 2026/05/12
Zhu ZhongquanChai HuaWang LipingWang JianZhou XiaoZhao DongXu BoFang YongjinChen XianguoZhang Lei - To identify dual-functional peptides from cod protein targeting oxidative stress and inflammation by investigating their electronic structure-activity relationships through an integrated computational and experimental approach. - Source: PubMed
Publication date: 2026/05/08
Xin Xuan-YingPark SungkwonWang Hao-WenHur SunjinLi Xiang-ZiChoi Seongho - Paclitaxel-induced peripheral neuropathic pain (PIPNP) is a common and debilitating adverse effect of chemotherapy, with limited effective treatments. Electroacupuncture (EA) has demonstrated analgesic potential in various pain models, but its efficacy and mechanisms in PIPNP remain incompletely understood. This study aimed to evaluate the analgesic effect of EA in a murine model of PIPNP and investigate whether its mechanism involves modulation of the TLR4/P2X7-NLRP3 signaling pathway. A PIPNP model was established in male C57BL/6 J mice by intraperitoneal injection of paclitaxel (cumulative dose 8 mg/kg). Mice were randomly divided into control, PIPNP model, PIPNP with EA treatment at different intensities (0.5, 1.0, and 2.0 mA), and sham EA groups. Mechanical allodynia and thermal hyperalgesia were assessed using von Frey filaments and hot plate tests, respectively. Immunofluorescence staining and western blotting were employed to analyze the expression of pain-related neurotransmitters (substance P, CGRP, p75) and key components of the TLR4/P2X7-NLRP3 signaling pathway in plantar tissues, dorsal root ganglia (DRG), and spinal cord. EA treatment, particularly at 1.0 mA, significantly alleviated paclitaxel-induced mechanical allodynia and thermal hyperalgesia. Paclitaxel administration upregulated substance P, CGRP, and p75 in plantar tissues and activated the TLR4/P2X7-NLRP3 signaling pathway in DRG and spinal cord, as evidenced by increased expression of TLR4, P2X7, NLRP3, NF-κB, IL-1β, and IL-18. EA intervention markedly suppressed these changes, indicating its role in inhibiting neuroinflammation and modulating pain-related signaling. EA exerts analgesic effects in paclitaxel-induced neuropathic pain by attenuating the activation of the TLR4/P2X7-NLRP3 signaling pathway and reducing the expression of pain-related neurotransmitters. - Source: PubMed
Publication date: 2026/05/12
Zhou Yuan-XiWang Man-NiXin Juan-JuanTan Jing-WeiSang XiaoZhao Yu-Xue