目的 探究特应性皮炎（atopic dermatitis， AD）患者血清C型凝集素结构域家族4成员G（C-type lectin domain family 4 member G，CLEC4G）水平及其临床价值。 方法 收集60例AD患者（观察组）和29例对照者（对照组）血液样本，检测样本中CLEC4G、白细胞介素-33（interleukin-33，IL-33）、总免疫球蛋白E（total IgE，tIgE）、特异性免疫球蛋白E（specific IgE，sIgE）及嗜酸性粒细胞水平；分析CLEC4G水平与AD患者临床资料及IL-33间的相关性；采用logistic回归分析CLEC4G、IL-33等指标评估AD发病的风险。 结果 与对照组相比，观察组患者血清CLEC4G水平显著降低［（359.4 ± 57.3）pg/mL vs （521.8 ± 48.1）pg/mL］；CLEC4G水平在儿童期、青少年与成年期及男、女性AD患者中均差异无统计学意义（P > 0.05）；与tIgE ≤ 100 kU/L组相比，CLEC4G水平在100 ~ 200 kU/L组、tIgE ≥ 200 kU/L组患者中显著降低，但在100 ~ 200 kU/L组、tIgE ≥ 200 kU/L组间无显著差异；血清CLEC4G水平只在AD病情中度组中显著降低，在其他组间差异无统计学意义（P > 0.05）；IL-33在观察组患者血清中水平升高，但CLEC4G与IL-33间无显著相关性（r = 0.090，P = 0.495）；年龄小于14岁、IL-33是AD发病的危险因子，OR值分别为2.756、1.241，95% CI分别为1.076 ~ 7.060、1.030 ~ 1.495；而CLEC4G为AD发病的保护因子（OR = 0.890，95%CI：0.809 ~ 0.979）。 结论 CLEC4G可能是独立于IL-33介导AD发病的保护因子。

Objective To investigate the serum C?type lectin domain family 4 member G（CLEC4G） level and its clinical value in patients with Atopic Dermatitis （AD）. Methods The blood samples of 60 AD patients and 29 control patients were collected， and CLEC4G， Interleukin?33 （IL?33）， total immunoglobulin E （tIgE）， specific IgE （specific IgE）， and eosinophil levels were detected. The correlation between CLEC4G level and clinical data of AD patients and IL?33 was analyzed. The risk of AD was evaluated by Logistic regression analysis of CLEC4G， IL?33 and other indicators. Results Compared with the control group， the serum CLEC4G level in AD patients was significantly decreased （359.4 ± 57.3 vs. 521.8 ± 48.1）pg/mL. There was no significant difference in CLEC4G level between childhood， adolescent and adult， male and female AD patients. Compared with tIgE ≤ 100 kU/L group，CLEC4G level was significantly decreased in 100 ~ 200 kU/L group and tIgE ≥ 200 kU/L group， but there was no significant difference between 100 ~ 200 kU/L group and tIgE ≥ 200 kU/L group. Serum CLEC4G level decreased significantly only in the moderate AD group， but had no significant difference among the other groups. The serum level of IL?33 was increased in AD patients， but there was no significant correlation between CLEC4G and IL?33 （r = 0.090， P = 0.495）. Age less than 14 years old and IL?33 were risk factors for the incidence of AD， with OR values of 2.756 and 1.241，95%CI of 1.076 ~ 7.060 and 1.030 ~ 1.495， respectively. CLEC4G was a protective factor for AD （OR = 0.890，95%CI：0.809 ~ 0.979）. Conclusion CLEC4G may be a protective factor independent of IL?33 mediated AD pathogenesis.