目的：探讨糖尿病神经病变患者角膜上皮下朗格汉斯细胞(Langerhans cell，LCs)与神经纤维病理改变的关系，分析其发病机制，并提出免疫机制在此过程中的可能作用。

方法：选取60例糖尿病神经病变患者和32例健康对照者，分析角膜神经纤维形态、数量、长度、角膜知觉和LC细胞密度，并分析二者的相关性。

结果：糖尿病神经病变患者角膜神经纤维数量和长度、分支数量明显降低，神经纤维弯曲度明显增加。糖尿病神经病变患者角膜中央和周边上皮下的LC密度与正常对照组相比升高(P<0.05)。同时相关性分析结果显示：LC密度和神经纤维密度(r=0.461，P=0.011)、长度(r=0.519，P=0.002)间存在线性相关。同时糖尿病神经病变患者角膜中央的知觉较对照组明显减退(P<0.05)。

结论：糖尿病神经病变患者角膜下神经纤维明显受损，角膜知觉减退，LC细胞数量增加，提示这种改变可能是免疫机制介导所致。

AIM: To study the relation between corneal epithelium Langerhans cells(LCs)and pathological changes of nerve fibers in patients with diabetic peripheral neuropathy in order to further analyze the pathogenesis and find the possible role of immune mechanism in this process.

METHODS: We selected 60 patients with diabetic neuropathy and 32 healthy controls to observe the morphology, number and length of corneal nerve fibers, corneal central sensation and the cell density of LCs to analyze the correlation of the two.

RESULTS: The number, length and the number of branches of corneal nerve fibers obvious declined in the patients with diabetic neuropathy. The curling degree of nerve fiber of diabetes group was obviously increased. The density of LCs at corneal central and peripheral areas in patients with diabetic neuropathy significantly increased compared to those of normal control group(P<0.05). The correlation analysis results showed that there were linear correlation between LCs and nerve fiber density(r =0.461, P=0.011), LCs and nerve fiber length(r=0.519, P=0.002). And corneal central sensation decreased obviously in patients with diabetic neuropathy compared to that in normal control(P<0.05).

CONCLUSION: In patients with diabetic neuropathy, the nerve fibers are significantly impaired, corneal sensation decreases and number of LCs significantly increases, which suggests that the changes might be mediated by the immune mechanism.