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The researchers reported that dsRNA from damaged skin activates TLR3, promoting hair follicle regeneration, while TLR3-deficient animals fail to initiate this process, suggesting potential therapeutic approaches for hair neogenesis.

This study found that the TLR3 L412F genetic variant is associated with severe viral infections, especially CMV, and immune dysfunction in a subgroup of chronic mucocutaneous candidiasis patients.

This study found that maternal consumption of a western diet in mice led to toxic milk production, causing inflammation and alopecia in nursing neonates due to Toll-like-receptor activation.

This study found that self-noncoding dsRNA activates TLR3 to stimulate intrinsic retinoic acid synthesis, promoting new hair follicle formation in wounded mice and showing similar gene expression changes in humans treated with rejuvenation lasers.

In this study, photodynamic therapy significantly reduced inflammatory acne lesions and sebum secretion, possibly by inducing apoptosis in sebaceous glands and down-regulating TLR-2 and TLR-4 expression.

In this study, TLR1 gene polymorphism rs4833095 was significantly associated with increased susceptibility to alopecia areata in the Korean population.

This study found that glioblastoma cancer stem cells avoid immune suppression by downregulating TLR4, and restoring TLR4 signaling may reduce tumor growth and self-renewal.

In this study, researchers found that using bioinspired nanovesicles derived from inflammation memory-activated epidermal stem cells effectively promoted healing in diabetic wounds by reprogramming neutrophils to an anti-inflammatory phenotype in both laboratory and animal models.

In this mouse study, researchers found that the Jieduquyuziyin prescription may lessen lupus-like symptoms and atherosclerosis by inhibiting TLR9/MyD88 signaling and promoting cholesterol efflux.

TLR7-based compounds may help manage chemotherapy-induced hair loss.

In this study involving adult mice, the researchers identified that double-stranded RNA-mediated activation of toll-like receptor 3 stimulates wound-induced hair neogenesis, potentially reflecting mechanisms used in facial rejuvenation treatments.

This study found that dracorhodin perchlorate improved wound healing in diabetic rats by regulating the TLR4 pathway and related inflammatory factors.

This study found that activating Toll-like receptor 3 in periodontal ligament stem cells enhanced their stem cell and immunosuppressive properties, potentially supporting effective periodontal tissue regeneration.

This study found that stimulating toll-like receptor 5 via mucosal delivery of a flagellin-containing fusion protein effectively extended lifespan and enhanced healthspan in mice, including improved bone density and cognitive capacity.

This study found that TLR2 expression in hair follicle stem cells is crucial for hair follicle maintenance and regeneration, with TLR2-dependent activation potentially offering new therapeutic approaches for hair loss prevention through mechanisms involving immune pathways and CEP administration.

This study found that expressions of TLR-3, TLR-7, TLR-8, and TLR-9 were significantly higher in alopecia areata patients compared to healthy controls, indicating a potential role in disease autoimmunity.

In this animal study, AGO (agomelatine) effectively alleviated testosterone-induced benign prostatic hyperplasia in rats by reducing oxidative stress and inflammation, indicating its potential as a therapeutic option for managing BPH through specific signaling pathways.

This study found that toll-like receptor 9 plays a previously unrecognized role in sensing skin injury and influencing tissue repair and regeneration in adult mice by modulating γδT cell migration.

This study found that TLR2 and its ligand CEP are crucial for maintaining hair follicle health and stimulating hair growth, with deficiencies observed in aging and obesity potentially reducing regeneration.

This study found that activating Toll-like receptor 3 signaling in periodontal ligament stem cells may enhance their immunomodulatory properties, suggesting potential implications for future stem cell therapy applications.

This study found that tissue damage in adult mice triggers the release of mitochondrial DNA, which activates the TLR9 pathway and influences hair regeneration by recruiting gamma delta T cells, ultimately affecting healing outcomes such as fibrosis.

This study found that TLR2 in hair follicle stem cells is crucial for maintaining hair health and regeneration, and its decrease in aging and obesity may impair hair growth, suggesting that stimulation through its ligand carboxyethylpyrrole could offer new therapeutic avenues.

This study found that TLR2 is crucial for maintaining hair follicle health and regeneration, and its stimulation by the metabolite CEP may promote hair growth, while decreases in TLR2 and CEP in aging and obesity may hinder hair growth.

This study suggests that autophagy is essential for regulating TLR3-mediated regenerative processes in human keratinocytes.

This review highlights the role of the receptor TLR4 in cellular aging and age-related diseases, suggesting it as a potential therapeutic target due to its contribution to persistent inflammation and symptom regulation in these conditions.

In this mouse study, aerobic exercise was found to protect the intestinal mucosal barrier in obstructive jaundice by inhibiting the HMGB1 / TLR4 / NF-κB signaling pathway through the H2S / CSE system.

This study found that oral administration of Flammulina velutipes polysaccharide reduced tumor volume and improved survival in mice by modulating macrophage polarization and enhancing antitumor immune responses.

This review discusses recent advances in understanding acne pathobiology, highlighting the potential for developing new customized therapies, but it reports no new clinical findings.

In this study, researchers found that mitochondrial complex I plays a crucial role in regulating innate immunity and bone remodeling, with Ndufs4 deletion causing systemic inflammation and osteopetrosis through various metabolic shifts and cellular mechanisms.