Department of Dermatology, Huashan Hospital, Fudan University, 12 Wulumuqi Zhong Road, Shanghai, 200040, PR China.
Br J Dermatol. 2016 Jun;174(6):1318-26. doi: 10.1111/bjd.14416. Epub 2016 May 4.
Vitiligo is a skin disorder characterized by loss of melanocytes from the epidermis. A recent study reported that CXCL10 is critical for the progression and maintenance of depigmentation in a mouse model of vitiligo, but there is very limited clinical data regarding this issue and little is known about the dynamic changes or correlations with disease severity of these chemokines throughout the disease course.
To present clinical data that supports and identifies the pathway of CXCR3 and its ligands in T-lymphocytic cell recruitment in vitiligo.
Cytometric bead array, flow cytometry, quantitative real-time polymerase chain reaction and immunohistology were used to examine their systemic and local expression in 80 patients with vitiligo and 40 controls.
We showed that serum CXCL9 and CXCL10 were significantly elevated in patients with vitiligo and were higher in patients in progressive stages than in stable stages. The relative expression of CXCR3 mRNA in peripheral blood mononuclear cells was higher in vitiligo. There were higher percentages of both circulating CXCR3(+) CD4(+) and CXCR3(+) CD8(+) T cells in patients with progressive vitiligo compared with controls, while only the expression of CXCR3(+) CD8(+) T cells increased in patients with stable vitiligo. Histological findings also demonstrated an abundance of CXCR3(+) cells within vitiligo lesions. Furthermore, serum CXCL10 levels were associated with Vitiligo Area Scoring Index scores of patients with progressive vitiligo and were reduced after successful treatment.
The CXCL10/CXCR3 axis mediates T-cell recruitment into the skin in progressive vitiligo. Blocking this chemotactic mechanism may present a new form of therapy. Serum CXCL10 may be a novel biomarker in monitoring disease activity and guiding treatment of progressive vitiligo.
白癜风是一种以表皮黑色素细胞丧失为特征的皮肤疾病。最近的一项研究报道称，趋化因子（C-X-C 基元）配体 10（CXCL10）在白癜风的小鼠模型中对脱色素的进展和维持至关重要，但关于这个问题的临床数据非常有限，而且对于这些趋化因子在整个疾病过程中的动态变化或与疾病严重程度的相关性知之甚少。
提供支持并确定趋化因子受体 3（CXCR3）及其配体在白癜风中 T 淋巴细胞募集途径的临床数据。
使用流式细胞术、酶联免疫吸附试验、实时聚合酶链反应和免疫组织化学检测了 80 例白癜风患者和 40 例对照者的血清和皮损中这些趋化因子的系统和局部表达。
我们发现，白癜风患者的血清 CXCL9 和 CXCL10 明显升高，进展期患者的水平高于稳定期患者。白癜风患者外周血单个核细胞中 CXCR3mRNA 的相对表达水平较高。与对照组相比，进展期白癜风患者的循环 CXCR3(+)CD4(+)和 CXCR3(+)CD8(+)T 细胞比例较高，而稳定期白癜风患者只有 CXCR3(+)CD8(+)T 细胞表达增加。组织学发现也表明 CXCR3(+)细胞在白癜风皮损中丰富存在。此外，进展期白癜风患者的血清 CXCL10 水平与白癜风面积评分指数（VASI）评分相关，且成功治疗后其水平降低。
趋化因子（C-X-C 基元）配体 10（CXCL10）/趋化因子受体 3（CXCR3）轴介导进展期白癜风患者的 T 细胞向皮肤募集。阻断这种趋化机制可能为新的治疗方法提供依据。血清 CXCL10 可能是监测疾病活动和指导进展期白癜风治疗的新型生物标志物。
