据一篇发表于本周Journal of Clinical Investigation的一篇研究报告称，在某些慢性炎症性疾病（如牛皮癣、哮喘等）中，如果Th22细胞(免疫细胞的一种)失去控制，将使这些慢性疾病的症状发生恶化。
据Dr Carsten Schmidt-Weber介绍，近些年，由于人们生活方式的转变，患慢性皮肤或呼吸道疾病的人越来越多，这些疾病严重影响人们的生活。研究人员在分析牛皮癣，湿疹和过敏性接触性皮炎的皮肤样品过程中发现了Th22细胞。
Th22细胞是一类T辅助细胞(T-helper cell)，当机体感染病毒或细菌等病原体后，T辅助细胞能够激活其他免疫细胞，并且还能帮助机体控制炎症对抗感染。研究人员通过分析Th22细胞中的各类分子，发现了一种重要的信号分子——白细胞介素22(IL-22)，当发生炎症或感染时，IL-22对组织发出预警，使组织作好识别和攻击病原体的准备。
在这项新研究中，Th22在监督和协调引起炎症的免疫细胞过程中起特殊的作用。而在慢性以及过敏性炎症疾病(如牛皮癣、过敏性湿疹等)中，Th22功能丧失将使慢性炎症疾病恶化。课题组所发现的这组新的T辅助细胞，或许在未来可以作为治疗慢性炎症疾病的靶标。（生物谷Bioon.com）
生物谷推荐原始出处：
J. Clin. Invest. doi:10.1172/JCI40202.
Th22 cells represent a distinct human T cell subset involved in epidermal immunity and remodeling
Stefanie Eyerich1, Kilian Eyerich2, Davide Pennino2, Teresa Carbone2, Francesca Nasorri2, Sabatino Pallotta3, Francesca Cianfarani4, Teresa Odorisio4, Claudia Traidl-Hoffmann5, Heidrun Behrendt5, Stephen R. Durham6, Carsten B. Schmidt-Weber1 and Andrea Cavani2
1Molecular Immunology, Department of Allergy and Clinical Immunology, National Heart and Lung Institute, Imperial College, London, United Kingdom.
2Laboratory of Immunology,
3Division of Dermatology, and
4Laboratory of Cellular and Molecular Biology, Istituto Dermopatico dell’Immacolata, IRCCS, Rome, Italy.
5Division of Environmental Dermatology and Allergy, Helmholtz Center Munich/Technische Universit?t Munich and ZAUM — Center for Allergy and Environment, Technische Universit?t Munich, Munich, Germany.
6Upper Respiratory Medicine, Department of Allergy and Clinical Immunology, National Heart and Lung Institute, Imperial College, London, United Kingdom.
Th subsets are defined according to their production of lineage-indicating cytokines and functions. In this study, we have identified a subset of human Th cells that infiltrates the epidermis in individuals with inflammatory skin disorders and is characterized by the secretion of IL-22 and TNF-α, but not IFN-γ, IL-4, or IL-17. In analogy to the Th17 subset, cells with this cytokine profile have been named the Th22 subset. Th22 clones derived from patients with psoriasis were stable in culture and exhibited a transcriptome profile clearly separate from those of Th1, Th2, and Th17 cells; it included genes encoding proteins involved in tissue remodeling, such as FGFs, and chemokines involved in angiogenesis and fibrosis. Primary human keratinocytes exposed to Th22 supernatants expressed a transcriptome response profile that included genes involved in innate immune pathways and the induction and modulation of adaptive immunity. These proinflammatory Th22 responses were synergistically dependent on IL-22 and TNF-α. Furthermore, Th22 supernatants enhanced wound healing in an in vitro injury model, which was exclusively dependent on IL-22. In conclusion, the human Th22 subset may represent a separate T cell subset with a distinct identity with respect to gene expression and function, present within the epidermal layer in inflammatory skin diseases. Future strategies directed against the Th22 subset may be of value in chronic inflammatory skin disorders.
