Pucheu-Haston Cherie M, Bizikova Petra, Marsella Rosanna, Santoro Domenico, Nuttall Tim, Eisenschenk Melissa N C
Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University, 1909 Skip Bertman Drive, Baton Rouge, LA, 70803, USA.
Vet Dermatol. 2015 Apr;26(2):124-e32. doi: 10.1111/vde.12205.
The development of atopic dermatitis (AD) and other cutaneous hypersensitivities involves the activation and differentiation of allergen-specific lymphocytes. Although hypersensitivity is often considered to be a 'T-helper 2-polarized' lymphocyte response, recent evidence suggests that clinical disease is associated with the development of multiple lymphocyte phenotypes.
The purpose of this paper is to review recent advances in the understanding of the roles of lymphocytes, cytokines and noncytokine factors in the pathogenesis of canine AD.
Citation databases, abstracts and proceedings from international meetings published between 2001 and 2013 were reviewed in this update. Where necessary, older articles were included for background information.
The development of canine AD is associated with changes in both cutaneous and circulating lymphocyte populations. These lymphocyte responses are characterized by the production of a complex variety of cytokines, including not only T-helper 2 but also T-helper 1, T-helper 17 and regulatory T-cell responses. In addition, microarray gene expression analysis has enabled the identification of a number of noncytokine factors that appear to be associated with atopic inflammation. These include the calcium-binding protein S100A8, serum amyloid A and a number of protease inhibitors, as well as genes involved in epidermal barrier formation, innate immunity receptors, cell cycle proteins and apoptosis.
The development of AD in dogs is characterized by the development of a delicate balance between a variety of T-cell phenotypes and inflammatory mediators, including cytokines, chemokines and noncytokine factors.
特应性皮炎（AD）和其他皮肤超敏反应的发生涉及变应原特异性淋巴细胞的激活和分化。尽管超敏反应通常被认为是一种“T辅助2型极化”淋巴细胞反应，但最近的证据表明，临床疾病与多种淋巴细胞表型的发展有关。
本文旨在综述对淋巴细胞、细胞因子和非细胞因子在犬AD发病机制中的作用的最新认识进展。
在本次更新中，对2001年至2013年间发表的文献数据库、国际会议摘要和会议记录进行了综述。必要时纳入较旧的文章以获取背景信息。
犬AD的发生与皮肤和循环淋巴细胞群体的变化有关。这些淋巴细胞反应的特征是产生多种复杂的细胞因子，不仅包括T辅助2型细胞因子，还包括T辅助1型、T辅助17型细胞因子和调节性T细胞反应。此外，微阵列基因表达分析已能够鉴定出一些似乎与特应性炎症相关的非细胞因子。这些因子包括钙结合蛋白S100A8、血清淀粉样蛋白A和一些蛋白酶抑制剂，以及参与表皮屏障形成、固有免疫受体、细胞周期蛋白和细胞凋亡的基因。
犬AD的发生特征是多种T细胞表型与炎症介质（包括细胞因子、趋化因子和非细胞因子）之间形成微妙的平衡。
