MyD88 Blocking Peptide
- Known as:
- MyD88 Blocking Peptide
- Catalog number:
- 3244RBP-50
- Product Quantity:
- 50 ug
- Category:
- -
- Supplier:
- Biovis
- Gene target:
- MyD88 Blocking Peptide
Related genes to: MyD88 Blocking Peptide
- Gene:
- MYD88 NIH gene
- Name:
- MYD88 innate immune signal transduction adaptor
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 3p22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-12-23
- Date modifiied:
- 2019-04-23
Related products to: MyD88 Blocking Peptide
Related articles to: MyD88 Blocking Peptide
- Wound-induced hair follicle neogenesis (WIHN) represents a remarkable regenerative phenomenon observed in adult mammalian skin (predominantly studied in mice), in which large full-thickness wounds bypass fibrotic scarring to generate fully functional hair follicles. This process reflects the context-dependent reactivation of embryonic morphogenetic programs, driven by a coordinated tripartite immune-microbial-epithelial axis (defined here as the integrated multi-directional signaling network among localized immune cells, epithelial stem cells, and the skin microbiota/fibroblasts). Mechanistically, γδ T cells initiate dermal fibroblast reprogramming through an FGF9-Wnt feed-forward loop, while macrophages promote AKT/β-catenin signaling in Lgr5 epithelial stem cells via TNF-α-driven non-canonical pathways. Regulatory T cells (Tregs) further support follicular morphogenesis by delivering Jagged1/Notch signals. In parallel, the skin microbiota acts as a key amplifier of regeneration, modulating the wound microenvironment through the IL-1β/MyD88 signaling axis. Taken together, WIHN illustrates the remarkable functional plasticity of immune signaling, which can be repurposed from host defense to orchestrating tissue regeneration. By elucidating this dynamic murine skin-immune dialogue, this mini-review provides a conceptual framework for speculative precision immunomodulatory therapies and emerging translational approaches-such as laser-assisted tissue remodeling-aimed at treating inflammatory and scarring alopecia, as well as achieving scarless and functionally restorative wound healing. - Source: PubMed
Publication date: 2026/07/15
Ma Ying-MingShen WeiXie Xiao-LeiTang Shun-LiWu YuanZhong Hua-JieYan QiangSun Hui - The immune-excluded tumor immune microenvironment (TIME) limits responses to ICIs. Cancer-associated fibroblasts are the most abundant stromal population and key regulators of immune suppression; however, the upstream cues that program pathogenic CAF states and the mechanisms of the immune-excluded TIME remain poorly defined. Here, by combining single-cell RNA sequencing and functional validation, we report that tumor cell-released autophagosome (TRAP) programs inflammatory CAFs (iCAFs) and triggers cathepsin L-dependent intracellular cleavage of C3 into C3a via the HSP70-TLR4-MyD88-ERK/p38 pathway. iCAF-derived C3a affects C3a on TAMs, promotes TAM accumulation in the iCAF-rich stroma, limits TIL trafficking into tumor nests, and reinforces an immune-excluded TIME. Disrupting the TRAP-iCAF-C3a/C3aR axis remodels the immune-excluded TIME and sensitizes tumors to anti-PD-L1 therapy. In clinical cohorts, plasma TRAP and C3a levels increased with disease stage, and their combination improved the discrimination of patients with breast cancer from controls (AUC = 0.96). These data define a TRAP-driven stromal-immune circuit that promotes immune exclusion and suggest that the C3a-C3aR axis is a potential target for enhancing ICI efficacy. - Source: PubMed
Publication date: 2026/07/29
Wang XuruWei YitingWu ChengdongZhou XiaoheSun XiaotongDu XiaoyueChen JinpengChen JingZhang WenqiBo XiangweiZhang YunpengShen BoWen ShaodiWang Lixin - The gut microbiota influences host metabolism, but the mechanisms of lipid uptake from food remain mysterious. Here we used stable isotope-labelled tracers in gnotobiotic mouse models, which revealed that host uptake of dietary lipids depends on microbial colonization. Systemic lipid metabolism modelling predicted that the gut microbiota restricts intestinal lipid absorption, and labelled lipid administration verified that the gut contents of microbiota-colonized mice contained up to 12-fold more lipids than those of germ-free animals. A combination of lipidomics and proteomics showed that gut microbes trigger Myd88 signalling, leading to a downregulation of hepatic Cyp7b1 activity and increased taurocholate production. Taurocholate stimulates phospholipase A1 activity in bile, causing the degradation of phosphatidylcholine that is essential for luminal micelle formation and lipid uptake. A diverse microbiome was associated with lower phosphatidylcholine content. This previously unrecognized host-gut microbiota interplay via enzymes in bile could provide future targets to modulate dietary lipid absorption. - Source: PubMed
Publication date: 2026/07/29
Brunner SarahPlagge JohannesZimmermann-Kogadeeva MariaHöring MarcusLiebisch GerhardBasic MarijanaBolsega SilviaJanssen Klaus-PeterSlack Emmavon Gamm SophiaViehof-Beckmann AlinaClavel ThomasZimmermann MichaelHeeren JoergGiansanti PieroWeiss Anna SHermeling SvenDupont AlineUllrich Anna-LenaJokisch FlorianSeeliger ClaudineBleich AndreHidrobo MariaStecher BärbelColeman Olivia IMoresi ClaudiaGreter GiorgiaArnoldini MarkusScheiber JosefMatysik SilkeKlingenspor MartinKüster BernhardHaller DirkBurkhardt RalphKuipers FolkertEcker Josef - Pathogens, tissue damage, and cellular stress are detected by innate immune sensor molecules to drive inflammatory signaling and cell death. Mutations in the sensor NLRP1 are associated with inflammatory disease, but the regulation of this sensor is not well understood. Here, we find that LPS, a TLR4 ligand and canonical activator of innate immunity, inhibits NLRP1-mediated caspase activation, IL-18 release, and inflammatory cell death, PANoptosis. This inhibition requires TRIF but not MyD88, implicating TRIF-dependent TLR signaling. IRF3 is also required, suggesting an essential role for type I IFN signaling. Indeed, IFN-β production or treatment with exogenous IFN-α or IFN-β inhibits NLRP1-dependent PANoptosis in mouse bone marrow-derived macrophages and human macrophages and monocytes. Mechanistically, Nlrp1b/NLRP1 expression is significantly reduced in LPS- or type I IFN-treated cells. Overall, our study identifies a TLR4-TRIF-IRF3 signaling axis that induces type I IFNs to negatively regulate NLRP1 transcription, thereby blocking NLRP1-driven, caspase-1/caspase-8/RIPK3-dependent PANoptosis. These findings suggest type I IFNs as a potential therapeutic strategy for NLRP1-driven inflammatory diseases. - Source: PubMed
Publication date: 2026/07/29
Sharma Bhesh RajMummareddy HarisankeerthChadchan Sangappa BSarkar RomanEi Farran Chadi AKanneganti Thirumala-Devi - Periodontitis is a chronic immunoinflammatory disease characterized by site-specific destruction of the tooth-supporting tissues and marked heterogeneity in disease susceptibility, progression, and response to therapy. While dysbiotic subgingival biofilms initiate disease, microbial burden alone cannot explain the persistence of inflammation or the limited predictability of regenerative outcomes. Increasing evidence implicates innate immune dysregulation, particularly Toll-like receptor (TLR) signaling, as a central determinant of periodontal disease behavior. This narrative review synthesizes current evidence on TLR signaling in periodontal tissues, emphasizing the concept that chronic periodontitis is sustained by biased downstream signaling integration rather than uniform receptor overactivation. We discuss how persistent dominance of pro-inflammatory, MyD88-dependent pathways, coupled with insufficient engagement of regulatory and resolution-associated programs, promotes inflammatory persistence, osteoimmune imbalance, and functional impairment of periodontal stromal and stem/progenitor cells. Cell-type-specific responses to TLR activation, genetic modulation of signaling thresholds, and reciprocal interactions between innate immunity and dysbiosis are examined as key contributors to disease heterogeneity. We further explore the implications of biased TLR signaling for periodontal regeneration, proposing that regenerative failure reflects an unfavorable inflammatory signaling milieu rather than depletion of regenerative cell populations. Finally, emerging experimental strategies for interrogating and modulating TLR signaling networks-including localized immune modulation and targeted protein degradation approaches-are discussed as mechanistic research tools rather than immediate therapeutic solutions. By reframing periodontitis as a disorder of maladaptive innate immune signaling integration, this review provides a unifying conceptual framework linking dysbiosis, host-response heterogeneity, and impaired regeneration, and defines priorities for future mechanistic and translational research. - Source: PubMed
Publication date: 2026/07/13
Mekhemar MohamedHassanein Fatma E AAbou-Bakr Asmaa