Atopic Dermatitis - Disease Etiology, Clinical Mgmt. by J. Esparza-Gordillo

By J. Esparza-Gordillo

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2005). Tenascin-C is upregulated in the skin lesions of patients with atopic dermatitis. 1, (October 2005), pp. Y. & Xie, M. (2007). Transient receptor potential channels as drug targets. 3, (March 2007), pp. M. D. (2010) The role of filaggrin in the atopic diathesis. Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology, Vol. 40, No. 965-972, ISSN 0954-7894. F. S. (2009) Filaggrin-deficient mice exhibit TH17dominated skin inflammation and permissiveness to epicutaneous sensitization with protein antigen.

1992b). Expression of functional diphtheria toxin receptors on highly toxin-sensitive mouse cells that specifically bind radioiodinated 36 Atopic Dermatitis – Disease Etiology and Clinical Management toxin. 6, (March 1992), pp. , Kubo, S. & Nakamura, Y. (1999). Mapping of a gene responsible for dermatitis in NOA (Naruto Research Institute Otsuka Atrichia) mice, an animal model of allergic dermatitis. 6, (August 1999), pp. , Bieber, T. Y. (2003). Immune mechanisms leading to atopic dermatitis. 6 Suppl, (December 2003), pp.

4, 5). No segregation was observed between hyper-IgE–emia and dermatitis in BALB/c x KOR mutant N2 mice. Furthermore, linkage analysis showed that both phenotypes are controlled by a same single recessive locus, and thus we designated the (a) (a) Phenotype segregation in the KOR colony. A pedigree of the KOR strain in which adjm mutant mice were first discovered (shown by arrows). The squares and circles represent males and females, respectively. The closed and open symbols represent affected and non-affected individuals, respectively.

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