吉林大学学报(医学版) ›› 2021, Vol. 47 ›› Issue (6): 1581-1587.doi: 10.13481/j.1671-587X.20210632
收稿日期:
2021-05-18
出版日期:
2021-11-28
发布日期:
2021-12-14
通讯作者:
刘丽
E-mail:lli01@jlu.edu.cn
作者简介:
车红明(1994-),女,吉林省松原市人,在读硕士研究生,主要从事小儿呼吸系统疾病基础和临床方面的研究。
基金资助:
Received:
2021-05-18
Online:
2021-11-28
Published:
2021-12-14
摘要:
腺病毒是一种无包膜的双链DNA病毒,目前已知其至少有90个基因型和70多个血清型,有A~G 共7个亚属,是引起儿童肺炎的常见病原体之一。儿童腺病毒肺炎的发病机制复杂,首先腺病毒通过与细胞表面的受体结合而实现病毒颗粒的内化、内吞作用或胞饮作用,最终被转运至核心孔进入细胞核完成复制并释放,这能够启动下游通路进行信号传导,刺激导致肺组织损伤的炎性细胞因子和趋化因子的大量释放,进而引起机能障碍。同时细胞免疫在腺病毒感染中发挥重要作用,Mφ、DC细胞、CD4+T淋巴细胞和CD8+T淋巴细胞等免疫细胞参与腺病毒感染。Mφ和DC细胞主要发挥免疫抗原的提呈功能,在适应性免疫过程中不可或缺,而免疫应答过程中有CD4+T淋巴细胞和CD8+T淋巴细胞参与。体液免疫与细胞免疫同时进行,其是抗原刺激B淋巴细胞产生抗体的一种免疫反应,主要由B淋巴细胞完成。现综述儿童腺病毒肺炎的发病机制,探讨通过阻断腺病毒入侵靶细胞、复制和抑制细胞因子的产生、体内诱导CD4+ T淋巴细胞和CD8+ T淋巴细胞产生或体外补充CD4+ T淋巴细胞及CD8+T淋巴细胞治疗儿童腺病毒肺炎的重要意义,为腺病毒肺炎的治疗提供依据。
中图分类号:
车红明,马瑜聪,张璐,石永娟,刘丽. 儿童腺病毒肺炎发病机制的研究进展[J]. 吉林大学学报(医学版), 2021, 47(6): 1581-1587.
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