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- The text analyzes the effectiveness of various animal models used to study atopic dermatitis (AD) in both traditional Chinese medicine (TCM) and Western medicine, highlighting how well these models reflect clinical symptoms.
- It discusses the strengths and weaknesses of different modeling methods, noting that while some models are consistent with AD characteristics, they may be costly and not fully capture the disease’s progression.
- The study suggests that integrating insights from both TCM and Western medicine could enhance the development of more accurate animal models for AD research.
Tissue-resident memory-like ILCs: innate counterparts of T cells.
Protein Cell
February 2020
Division of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, 230027, China.
Innate lymphoid cells (ILCs) are defined as lymphocytes that lack RAG recombinase and do not express diverse antigen receptors; however, recent studies have revealed the adaptive features of ILCs. Mouse cytomegalovirus (MCMV)- and cytokine-induced memory natural killer (NK) cells circulate in the blood and are referred to as conventional memory NK cells. In contrast, virus- and hapten-induced memory NK cells, hapten-induced memory ILC1s, and cytokine-induced memory-like ILC2s exhibit long-term residency in the liver or lung, and are referred to as tissue-resident memory ILCs.
View Article and Find Full Text PDFSite-specific regulation of oral mucosa-recruiting CD8 T cells in a mouse contact allergy model.
Biochem Biophys Res Commun
September 2017
Department of Molecular Immunology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, Japan. Electronic address:
Contact allergy is a T cell-mediated, delayed-type hypersensitivity generated by contact exposure of an allergen to the skin and mucosal surface. The clinical manifestations of allergic responses between the skin and oral mucosa vary and the differences in immunopathology have not been clarified. We generated hapten-induced contact hypersensitivity (CH) of the buccal mucosa (BM) in parallel studies with ear skin (ES) CH, and observed several characteristic findings of BM CH.
View Article and Find Full Text PDFDose-dependent role of claudin-1 in vivo in orchestrating features of atopic dermatitis.
Proc Natl Acad Sci U S A
July 2016
Laboratory of Biological Science, Graduate School of Frontier Biosciences and Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan;
Atopic dermatitis (AD) is a chronic inflammatory skin disease in humans. It was recently noted that the characteristics of epidermal barrier functions critically influence the pathological features of AD. Evidence suggests that claudin-1 (CLDN1), a major component of tight junctions (TJs) in the epidermis, plays a key role in human AD, but the mechanism underlying this role is poorly understood.
View Article and Find Full Text PDFDepletion of regulatory T cells in a hapten-induced inflammation model results in prolonged and increased inflammation driven by T cells.
Clin Exp Immunol
March 2015
Department of Immunopharmacology, Novo Nordisk A/S, Måløv, Denmark; Department of Veterinary Disease Biology, Section for Experimental Animal Models, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg, Denmark.
Regulatory T cells (Tregs ) are known to play an immunosuppressive role in the response of contact hypersensitivity (CHS), but neither the dynamics of Tregs during the CHS response nor the exaggerated inflammatory response after depletion of Tregs has been characterized in detail. In this study we show that the number of Tregs in the challenged tissue peak at the same time as the ear-swelling reaches its maximum on day 1 after challenge, whereas the number of Tregs in the draining lymph nodes peaks at day 2. As expected, depletion of Tregs by injection of a monoclonal antibody to CD25 prior to sensitization led to a prolonged and sustained inflammatory response which was dependent upon CD8 T cells, and co-stimulatory blockade with cytotoxic T lymphocyte antigen-4-immunoglobulin (CTLA-4-Ig) suppressed the exaggerated inflammation.
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