據(jù)一篇發(fā)表于本周Journal of Clinical Investigation的一篇研究報告稱,，在某些慢性炎癥性疾?。ㄈ缗Ｆぐ_,、哮喘等）中,，如果Th22細(xì)胞(免疫細(xì)胞的一種)失去控制，將使這些慢性疾病的癥狀發(fā)生惡化。
據(jù)Dr Carsten Schmidt-Weber介紹,，近些年,，由于人們生活方式的轉(zhuǎn)變，患慢性皮膚或呼吸道疾病的人越來越多,，這些疾病嚴(yán)重影響人們的生活,。研究人員在分析牛皮癬，濕疹和過敏性接觸性皮炎的皮膚樣品過程中發(fā)現(xiàn)了Th22細(xì)胞,。
Th22細(xì)胞是一類T輔助細(xì)胞(T-helper cell)，當(dāng)機體感染病毒或細(xì)菌等病原體后,，T輔助細(xì)胞能夠激活其他免疫細(xì)胞,，并且還能幫助機體控制炎癥對抗感染。研究人員通過分析Th22細(xì)胞中的各類分子,，發(fā)現(xiàn)了一種重要的信號分子——白細(xì)胞介素22(IL-22),，當(dāng)發(fā)生炎癥或感染時，IL-22對組織發(fā)出預(yù)警,，使組織作好識別和攻擊病原體的準(zhǔn)備,。
在這項新研究中，Th22在監(jiān)督和協(xié)調(diào)引起炎癥的免疫細(xì)胞過程中起特殊的作用,。而在慢性以及過敏性炎癥疾病(如牛皮癬,、過敏性濕疹等)中，Th22功能喪失將使慢性炎癥疾病惡化,。課題組所發(fā)現(xiàn)的這組新的T輔助細(xì)胞,，或許在未來可以作為治療慢性炎癥疾病的靶標(biāo)。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
