Tohoku University · Medicine
Professor Toshiya Takahashi's research lab focuses on the immunological mechanisms underlying chronic inflammatory skin diseases, particularly psoriasis and related disorders such as dissecting cellulitis of the scalp (PCAS). The lab investigates the role of endogenous host defense peptides—especially cathelicidin LL-37—in breaking self-tolerance to self-nucleic acids, thereby promoting innate immune activation through pattern recognition receptors. Using molecular and cellular approaches, including reporter cell lines and multi-omics techniques, the lab explores how damage-associated molecular patterns (DAMPs) and antimicrobial peptides synergize to drive interferon production and chronic inflammation. The lab also engages in translational research, evaluating therapeutic targets such as TNF inhibitors in treatment-resistant inflammatory skin conditions.
Figures are computed from collected data and may differ slightly.
Psoriasis is a systemic inflammatory disease caused by crosstalk between various cells such as T cells, neutrophils, dendritic cells, and keratinocytes. Antimicrobial peptides (AMPs) such as β-defensin, S100, and cathelicidin are secreted from these cells and activate the innate immune system through various mechanisms to induce inflammation, thus participating in the pathogenesis of psoriasis. In particular, these antimicrobial peptides enhance the binding of damage-associated molecular pattern
Several studies have suggested that interleukin (IL)-8 can serve as a biomarker for discrimination of skin sensitizers from nonsensitizers. We established a stable THP-1-derived IL-8 reporter cell line, THP-G8, which harbors SLO and SLR luciferase genes under the control of IL-8 and glyceraldehyde 3-phosphate dehydrogenase promoters, respectively. After 6 h treatment with chemicals, normalized SLO luciferase activity (nSLO-LA) was calculated by dividing SLO-LA by SLR-LA, and the fold induction o
Under homeostatic conditions the release of self-RNA from dying cells does not promote inflammation. However, following injury or inflammatory skin diseases such as psoriasis and rosacea, expression of the cathelicidin antimicrobial peptide LL37 breaks tolerance to self-nucleic acids and triggers inflammation. Here we report that LL37 enables keratinocytes and macrophages to recognize self-non-coding U1 RNA by facilitating binding to cell surface scavenger receptors that enable recognition by nu
Enantioselective and diastereoselective Darzens reaction mediated by chiral lithium amides was achieved between tert-butyl chloroacetate and aromatic aldehydes to give the corresponding trans-glycidic esters in up to 84% enantiomeric excess.
Perifolliculitis capitis abscedens et suffodiens (PCAS) or dissecting cellulitis is a rare condition presenting deep follicular occlusions, follicular ruptures and follicular infections in the scalp area with unknown etiology, which consequently cause primary neutrophilic cicatricial alopecia by the repeated follicular inflammation. PCAS is categorized as one of the "follicular occlusion tetrad" along with hidradenitis suppurativa, acne conglobata and pilonidal cyst. In the pathogenesis of the f
An active form of cathelicidin antimicrobial peptide, LL-37, has immunomodulatory and stimulatory effects, though the specific pathways are not clear. The purpose of this study was to identify the cellular pathways by which LL-37 amplifies the inflammation induced by damage-associated molecular patterns (DAMPs). We performed DNA microarray, reverse transcription polymerase chain reaction, immunoblotting, and proximity ligation assays using cultured keratinocytes treated with LL-37 and/or the DAM
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