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Temporal Dynamic Changes of Phenotypic Expression of Peripheral CD4 Cells during Environmental Allergen Challenge in an Experimental Model of Canine Atopic Dermatitis: A Pilot Study. The Journal of veterinary medical science / the Japanese Society of Veterinary Science [J Vet Med Sci] Journal article

 
Simpson A, Maeda S, Marsella R 
Temporal Dynamic Changes of Phenotypic Expression of Peripheral CD4 Cells during Environmental Allergen Challenge in an Experimental Model of Canine Atopic Dermatitis: A Pilot Study. [Journal Article]
J Vet Med Sci 2009 Sep; 71(9):1177-81.


The immunopathology behind atopic dermatitis (AD) involves a myriad of inflammatory cells and their mediators. Thymus and activation-regulated chemokine (TARC) plays a significant role in the inflammatory phase by recruiting CCR4(+) T(H)2 cells. In addition, CD25(+) activated T cells further propagate the allergic response after sensitization by producing cytokines. The purpose of this pilot study was to evaluate how exposure to a common allergen (house dust mite, HDM) would affect the proportions of circulating CD4(+)CCR4(+) T(H)2 cells and CD4(+)CD25(+)activated T cells in an experimental model of AD using high-IgE Beagles. In this experimental model, previously sensitized Beagles develop lesions and pruritus upon allergen challenge consisting of 3-day environmental exposure, 3 hours/day. Blood samples were obtained before, during, and after the end of challenge (days 0, 2, 4, and 17). Clinical signs were evaluated and scored at the same time points. Peripheral blood mononuclear cells (PBMCs) were isolated and used for flow cytometry to identify proportions of CD4(+)cells positive for either CCR4 or CD25 receptors. Both CD4(+)cell types (CD25(+) and CCR4(+)) peaked at day 17, when clinical signs had resolved. It is proposed that the increase of circulating CD4(+)CCR4(+) and CD4(+)CD25(+)cells most likely demonstrates the sensitization status of atopic individuals after environmental allergen challenge. Understanding of these two cell types could prompt additional research concerning therapeutic drugs for AD.



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