Basak Pinar Y, Adiloglu Ali K, Ceyhan Ali Murat, Tas Tekin, Akkaya Vahide B
Department of Dermatology, Faculty of Medicine, Suleyman Demirel University, Isparta, Turkey.
J Am Acad Dermatol. 2009 Feb;60(2):256-60. doi: 10.1016/j.jaad.2008.09.048. Epub 2008 Nov 20.
Alterations in cellular immunity, including CD4(+) T and CD8(+) T lymphocytes, have been proposed in the pathogenesis of vitiligo. There is also a proposed role for cytokines in the depigmentation observed in vitiligo. However, previous reports on the role of cytokines in the pathogenesis of vitiligo have been few in number.
The purpose of this investigation was to assess the role of the major cytokines produced by T-helper 1 and 2 cells as well as T-helper 17 and regulatory T cells in the pathogenesis of vitiligo.
Forty patients with vitiligo and 40 age- and sex-matched healthy control subjects were enrolled in the study. Serum interleukin (IL)-4, IL-6, IL-10, IL-17, interferon-gamma, tumor necrosis factor-beta, and transforming growth factor-beta levels were detected by enzyme-linked immunosorbent assay in both groups. The correlations of serum cytokine levels with age of onset, sex, duration of disease, type and activity of vitiligo, percentage of involved body area, Koebner positivity, family history, and the presence of associated autoimmune diseases were assessed.
Serum transforming growth factor-beta levels were significantly decreased in the vitiligo group compared with the control group (P = .004). No difference was detected between the patient and control groups in mean levels of serum IL-6, IL-10, and tumor necrosis factor-beta. In the patients with vitiligo, serum IL-17 levels were positively correlated with the extent of body area involvement (rho = 0.329, P = .038).
Tissue cytokines compared with those in the peripheral blood were not measured.
Although multiple factors have been implicated in the pathogenesis of vitiligo, reduced serum transforming growth factor-beta levels, as observed in patients in the current investigation, may contribute to enhanced cellular immunity. This may facilitate the occurrence of vitiligo by leading to diminished maturation of regulatory T cells, followed by impaired inhibition of inflammation.
白癜风发病机制中存在细胞免疫改变，包括CD4(+)T和CD8(+)T淋巴细胞。细胞因子在白癜风色素脱失中也被认为发挥一定作用。然而，以往关于细胞因子在白癜风发病机制中作用的报道数量较少。
本研究旨在评估辅助性T细胞1和2、辅助性T细胞17及调节性T细胞产生的主要细胞因子在白癜风发病机制中的作用。
本研究纳入40例白癜风患者及40例年龄和性别匹配的健康对照者。采用酶联免疫吸附测定法检测两组血清白细胞介素（IL）-4、IL-6、IL-10、IL-17、干扰素-γ、肿瘤坏死因子-β及转化生长因子-β水平。评估血清细胞因子水平与发病年龄、性别、病程、白癜风类型及活动度、受累体表面积百分比、同形反应阳性、家族史及相关自身免疫性疾病存在情况的相关性。
与对照组相比，白癜风组血清转化生长因子-β水平显著降低（P = 0.004）。患者组与对照组血清IL-6、IL-10及肿瘤坏死因子-β平均水平未检测到差异。在白癜风患者中，血清IL-17水平与体表面积受累程度呈正相关（rho = 0.329，P = 0.038）。
未检测组织细胞因子并与外周血中的进行比较。
尽管白癜风发病机制涉及多种因素，但本研究中患者血清转化生长因子-β水平降低可能导致细胞免疫增强。这可能通过导致调节性T细胞成熟减少，进而抑制炎症受损，促进白癜风的发生。
