Low number of regulatory T cells in skin lesions of patients with cutaneous lupus erythematosus

FOXP3型 白细胞介素2受体 医学 免疫学 单克隆抗体 流式细胞术 表型 自身免疫性疾病 免疫组织化学 红斑狼疮 系统性红斑狼疮 结缔组织病 发病机制 病理 抗体 疾病 免疫系统 生物 T细胞 基因 生物化学
作者
B Franz,Benedikt Fritzsching,Astrid Riehl,Nina Oberle,C.‐D. Klemke,J Sýkora,Sabine Quick,Christine Stumpf,Martin Hartmann,Alexander Enk,Thomas Ruzicka,Peter H. Krammer,Elisabeth Suri‐Payer,Annegret Kuhn
出处
期刊:Arthritis & Rheumatism [Wiley]
卷期号:56 (6): 1910-1920 被引量:131
标识
DOI:10.1002/art.22699
摘要

Abstract Objective To define the phenotype and function of CD4+,CD25+ regulatory T cells (Treg) in patients with cutaneous lupus erythematosus (CLE), a heterogeneous autoimmune disease characterized primarily by inflammatory skin lesions. Methods The number of Treg in skin specimens obtained from patients with various subtypes of CLE was investigated by immunohistochemical analysis, using anti‐Foxp3 and anti‐CD4 monoclonal antibodies. Furthermore, characterization of peripheral blood CD4+,CD25+ Treg from normal healthy donors and patients with CLE was carried out by flow cytometry, analyzing the expression of Foxp3 and Treg subpopulations. We also purified CD4+,CD25 high Treg obtained from patients with CLE and tested the sensitivity of these cells to CD95L‐mediated apoptosis. Results Quantitative analysis of CD4+ T cells in skin lesions from patients with CLE revealed that the number was similar to that in lesions from patients with other chronic inflammatory diseases, but the number of Foxp3+ Treg in CLE was significantly reduced. There was no correlation between disease subtype and the frequency of Foxp3+ Treg in the skin of patients with CLE. In peripheral blood, no significant differences were observed in the number and phenotype of CD4+,CD25+ Treg or in the sensitivity to apoptosis of CD4+,CD25 high Treg derived from patients with CLE and those derived from normal healthy donors. Conclusion These data suggest that an organ‐specific abnormality of Treg in the skin underscores the importance of analyzing Treg in the affected tissue. Such a local process might give insight into the pathogenic mechanisms of CLE and differs from a global peripheral dysfunction as reported for patients with a systemic manifestation of the disease.
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