ReviewEXCLI journal2021
Going, Toll-like receptors in skin inflammation and inflammatory diseases.
Review in EXCLI journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 31 citations in OpenAlex.
- IRAK4 degrader in hidradenitis suppurativa and atopic dermatitis: a phase 1 trial.Nature medicine · 2023Trial
- Atopic Dermatitis: New Targets and Emerging Systemic Therapies.American journal of clinical dermatology · 2026Review
- 25 Years of Cancer Immunoediting: Dendritic Cells and Macrophages Filled the Missing Gap.Cancers · 2026Review
- GPR108 Negatively Regulates TLR7 Signaling in Imiquimod-Induced Psoriasiform Dermatitis.Immunity, inflammation and disease · 2026Article
- Fire Needling Acupuncture Reduces Neutrophil Extracellular Traps (NETs) Formation and Inhibits TLR4/NF-κB/LCN2 Pathway in Psoriasis-Like Skin Lesions.Journal of inflammation research · 2026Article
- Review
- Advances in the pathogenesis of rosacea.Frontiers in immunology · 2025Review
- Anti-microbial impact of non-antibiotic agents; salicylic acid, N-acetylcysteine, and isotretinoin against Cutibacterium acnes in patients with acne vulgaris.Archives of dermatological research · 2024Observational
- Anti-Inflammatory Effects of Extracellular Vesicles fromInternational journal of molecular sciences · 2024Article
- Pathogenesis of Inflammation in Skin Disease: From Molecular Mechanisms to Pathology.International journal of molecular sciences · 2024Review
- Strong association of TLR2 and TLR3 polymorphisms with keratoacanthoma and common warts: a case-control study.Croatian medical journal · 2024Article
- Downregulation of circ_0035292 Alleviates LPS-Induced WI-38 Cell Injury via Targeting miR-494-3p/TLR4 Pathway in Infantile Pneumonia.Biochemical genetics · 2024Article
- The Features of Shared Genes among Transcriptomes Probed in Atopic Dermatitis, Psoriasis, and Inflammatory Acne: S100A9 Selection as the Target Gene.Protein and peptide letters · 2024Article
- Pattern-Recognition Receptors and Immunometabolic Reprogramming: What We Know and What to Explore.Journal of innate immunity · 2024Review
- Immune Homeostasis: A Novel Example of Teamwork.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Exploring the Pathogenesis and Mechanism-Targeted Treatments of Rosacea: Previous Understanding and Updates.Biomedicines · 2023Review
- Huangshui Polysaccharide Exerts Intestinal Barrier Protective Effects through the TLR4/MyD88/NF-Foods (Basel, Switzerland) · 2023Article
- Rosacea, microbiome and probiotics: the gut-skin axis.Frontiers in microbiology · 2023Review
- Langerhans Cells-Revising Their Role in Skin Pathologies.Journal of personalized medicine · 2022Review
- TLR4 polymorphisms as potential predictors of atopic dermatitis in Chinese Han children.Journal of clinical laboratory analysis · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Indian Ayurvedic physicians knew the concept of inflammation dating back to 1500 BC. The continuous progress in the immunology of inflammation has explained its undiscovered mechanisms. For example, the discovery of Toll-like receptor 4 (TLR4) in humans (1997) has revolutionized the field of infection biology and innate immunity. The laboratory mice have shown twelve TLRs and express TLR10 (CD290) as a disrupted pseudogene, and humans have ten functional TLRs. Now, it is well established that TLRs play a significant role in different infectious and inflammatory diseases. Skin inflammation and other associated inflammatory diseases, including atopic dermatitis (AD), acne vulgaris, and psoriasis, along with many skin cancers are major health problems all over the world. The continuous development in the immunopathogenesis of inflammatory skin diseases has opened the window of opportunity for TLRs in studying their role. Hence, the manuscript explores the role of different TLRs in the pathogenesis of skin inflammation and associated inflammatory diseases. The article starts with the concept of inflammation, its origin, and the impact of TLRs discovery on infection and inflammation biology. The subsequent section describes the burden of skin-associated inflammatory diseases worldwide and the effect of the geographical habitat of people affecting it. The third section explains skin as an immune organ and explains the expression of different TLRs on different skin cells, including keratinocytes, Langerhans cells (LCs), skin fibroblasts, and melanocytes. The fourth section describes the impact of TLRs on these cells in different skin-inflammatory conditions, including acne vulgaris, AD, psoriasis, and skin cancers. The article also discusses the use of different TLR-based therapeutic approaches as specific to these inflammatory skin diseases.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.