共信号分子CD28、ICOS在慢性乙型肝炎病人外周血T淋巴细胞表面的表达及意义

涂远航; 李珊珊; 陈策; 丁秀丽

doi:10.13898/j.cnki.issn.1000-2200.2022.03.006

共信号分子CD28、ICOS在慢性乙型肝炎病人外周血T淋巴细胞表面的表达及意义

Significance and expression of costimulatory molecules CD28 and ICOS in peripheral blood T lymphocyte of patient with chronic hepatitis B

摘要

摘要:
目的观察慢性乙型病毒性肝炎病人外周血T淋巴细胞表面共信号分子CD28、ICOS的表达水平，探讨CD28、ICOS在乙型肝炎病毒慢性感染中的意义。
方法选取慢性乙型病毒性肝炎病人56例作为观察组，纳入同期20名健康体检者作为对照组。流式细胞术检测受试者外周血T淋巴细胞表面CD28、ICOS的表达水平。
结果2组外周血CD4⁺、CD8⁺T淋巴细胞及CD4⁺/CD8⁺差异均无统计学意义(P>0.05)。观察组外周血CD4⁺CD28⁺T细胞、CD8⁺CD28⁺T细胞水平均明显低于对照组(P < 0.01)。2组CD4⁺ICOS⁺T细胞水平差异无统计学意义(P>0.05)；观察组CD8⁺ICOS⁺T细胞水平明显高于对照组(P < 0.01)。
结论慢性乙型肝炎病毒感染者同时存在免疫低下和免疫紊乱，主要与其T淋巴细胞表面共信号分子CD28、ICOS的表达异常有关。

Abstract:
ObjectiveTo observe the expression level of costimulatory molecules CD28 and ICOS on the surface of peripheral blood T lymphocyte in patient with chronic hepatitis B, and to explore the significance of CD28 and ICOS in chronic hepatitis B virus infection.
MethodsFifty-six patients with chronic hepatitis B were selected as the observation group, and 20 healthy examinees in the same period were included as the control group.Flow cytometry was used to detect the expression level of CD28 and ICOS on the surface of T lymphocyte in the subjects′ peripheral blood.
ResultsThere were no significant differences in the peripheral blood CD4⁺, CD8⁺T lymphocytes and the ratio of CD4⁺/CD8⁺ between the two groups(P>0.05).The levels of CD4⁺/CD28⁺T cells and CD8⁺/CD28⁺T cells in the peripheral blood in observation group were significantly lower than those in control group(P < 0.01).There was no significant difference in the level of CD4⁺ICOS⁺T cells between the two groups(P>0.05), and the level of CD8⁺ICOS⁺T cells in observation group was significantly higher than that in control group(P < 0.01).
ConclusionsPatients with chronic hepatitis B virus infection have both immunodeficiency and immune disorder, which are mainly related to the abnormal expression of the costimulatory molecules CD28 and ICOS on the surface of T lymphocyte.

HTML全文

参考文献(18)

施引文献

资源附件(0)