血浆 EBV 抗体、sCD26、sCD23 和 sCD30 水平与经典型卡波西肉瘤风险的关系。
Risk of classical Kaposi sarcoma by plasma levels of Epstein-Barr virus antibodies, sCD26, sCD23 and sCD30.
机构信息
Infections & Immunoepidemiology Branch, Division of Cancer Epidemiology & Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland, USA.
出版信息
Infect Agent Cancer. 2010 Oct 12;5:18. doi: 10.1186/1750-9378-5-18.
BACKGROUND
To clarify the immunological alterations leading to classical Kaposi sarcoma (cKS) among people infected with KS-associated herpesvirus (KSHV).
METHODS
In a population-based study of 119 cKS cases, 105 KSHV-seropositive controls, and 155 KSHV-seronegative controls, we quantified plasma soluble cluster of differentiation (sCD) levels and antibodies against Epstein-Barr virus nuclear antigen-1 (anti-EBNA-1) and viral capsid antigen (anti-VCA). Differences between groups in prevalence of low-tertile anti-EBNA-1 and high-tertile anti-VCA were compared by logistic regression. Continuous levels between groups and by presence of cKS co-factors among controls were compared by linear regression and Mann-Whitney-Wilcoxon methods.
RESULTS
Comparisons of cKS cases to seropositive controls and of seropositive to seronegative controls revealed no significant differences. However, controls with known cKS cofactors (male sex, nonsmoking, diabetes and cortisone use) had significantly lower levels of anti-EBNA (P = 0.0001 - 0.07) and anti-VCA (P = 0.0001 - 0.03). Levels of sCD26 were significantly lower for male and non-smoking controls (Padj ≤ 0.03), and they were marginally lower with older age and cortisone use (Padj ≤ 0.09).
CONCLUSIONS
Anti-EBV and sCD26 levels were associated with cofactors for cKS, but they did not differ between cKS cases and matched controls. Novel approaches and broader panels of assays are needed to investigate immunological contributions to cKS.
背景
阐明导致人类感染卡波西肉瘤相关疱疹病毒（KSHV）后出现经典卡波西肉瘤（cKS）的免疫学改变。
方法
在一项基于人群的研究中，我们对 119 例 cKS 病例、105 例 KSHV 血清阳性对照和 155 例 KSHV 血清阴性对照进行了研究，定量检测了血浆可溶性细胞分化（sCD）水平以及针对 EBV 核抗原-1（anti-EBNA-1）和病毒衣壳抗原（anti-VCA）的抗体。通过逻辑回归比较各组间低三分位数 anti-EBNA-1 和高三分位数 anti-VCA 的患病率差异。通过线性回归和 Mann-Whitney-Wilcoxon 方法比较组间连续水平和对照者中 cKS 合并因素的存在。
结果
将 cKS 病例与血清阳性对照进行比较，以及将血清阳性对照与血清阴性对照进行比较，均未发现显著差异。然而，具有已知 cKS 合并因素（男性、非吸烟、糖尿病和皮质激素使用）的对照者 anti-EBNA（P=0.0001-0.07）和 anti-VCA（P=0.0001-0.03）水平显著降低。男性和非吸烟对照者的 sCD26 水平显著降低（Padj≤0.03），并且随着年龄的增长和皮质激素的使用，其水平也略有降低（Padj≤0.09）。
结论
抗 EBV 和 sCD26 水平与 cKS 的合并因素相关，但在 cKS 病例与匹配对照者之间无差异。需要采用新方法和更广泛的检测试剂盒来研究免疫对 cKS 的贡献。
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