Ye Xiaohui, Zhang Zining, Jiang Yongjun, Han Xiaoxu, Wang Yanan, Zhang Min, Liu Jing, Geng Wenqing, Dai Di, Shi Wanying, Shang Hong
Key Laboratory of Immunology of AIDS, Ministry of Health, First Affiliated Hospital, China Medical University, Shenyang, Liaoning, China.
Viral Immunol. 2006 Summer;19(3):576-81. doi: 10.1089/vim.2006.19.576.
Our objective was to detect the expression of CD226 on natural killer (NK) cells and T cells, and to measure the amount of soluble CD226 in the plasma of HIV-infected individuals, in order to evaluate the function of CD226 in HIV infection. Thirty-four untreated HIV-1-infected patients and 26 normal controls were enrolled and three-color flow cytometry was used to detect the expression of CD226 on T lymphocytes and NK cells in whole blood samples taken from the patients and normal controls, and in HIV-1SF33-infected peripheral blood mononuclear cells (PBMCs). An enzymelinked immunosorbent assay (ELISA) was used to detect the level of soluble CD226 in the plasma of HIV-infected patients and normal controls and in the supernatant of HIV-1SF33-infected cells. The level of CD226 expression on CD3+, CD4+, and CD8+ T cells and on CD3- CD16+ NK cells of HIV-infected patients was significantly higher than that of normal controls (p < 0.01). The level of soluble CD226 in the plasma of HIV-infected patients was also significantly higher than that of normal controls (p < 0.01). After stimulation with HIV-1SF33, the level of CD226 expression on CD3+ T cells and CD3- CD16+ NK cells of cultured PBMCs reached peak values at 48 h, which was earlier than in uninfected control cells (72 h). The level of soluble CD226 in the supernatant of HIV- 1SF33-infected cell culture was higher than that of uninfected cells, and the level of soluble CD226 in the supernatant of HIV-1SF33-infected cells reached the peak value at 72 h, which was earlier than in uninfected control cells (96 h) but later than the time of peak CD226 expression on CD3+ T lymphocytes (48 h). We conclude that CD226 may be involved in the immune response to HIV infection and that further experiments are needed to find the function of CD226 in the pathogenesis of HIV infection.
我们的目标是检测自然杀伤(NK)细胞和T细胞上CD226的表达,并测量HIV感染个体血浆中可溶性CD226的量,以评估CD226在HIV感染中的功能。招募了34例未经治疗的HIV-1感染患者和26名正常对照,采用三色流式细胞术检测患者和正常对照全血样本以及HIV-1SF33感染的外周血单个核细胞(PBMC)中T淋巴细胞和NK细胞上CD226的表达。采用酶联免疫吸附测定(ELISA)检测HIV感染患者和正常对照血浆以及HIV-1SF33感染细胞上清液中可溶性CD226的水平。HIV感染患者CD3 +、CD4 +和CD8 + T细胞以及CD3 - CD16 + NK细胞上CD226的表达水平显著高于正常对照(p < 0.01)。HIV感染患者血浆中可溶性CD226的水平也显著高于正常对照(p < 0.01)。用HIV-1SF33刺激后,培养的PBMC中CD3 + T细胞和CD3 - CD16 + NK细胞上CD226的表达水平在48小时达到峰值,早于未感染对照细胞(72小时)。HIV-1SF33感染细胞培养上清液中可溶性CD226的水平高于未感染细胞,HIV-1SF33感染细胞上清液中可溶性CD226的水平在72小时达到峰值,早于未感染对照细胞(96小时),但晚于CD3 + T淋巴细胞上CD226表达的峰值时间(48小时)。我们得出结论,CD226可能参与了对HIV感染的免疫反应,需要进一步实验来发现CD226在HIV感染发病机制中的作用。