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回复 mtv982 的帖子
同意说法可能是错的, 至少不是完整的解释.因为直接证据来自小鼠模型研究.
e抗原会导致婴儿免疫系统耐受乙肝病毒的说法来自美国的一项研究:
http://www.cell.com/immunity/pdf/S1074-7613(16)30137-6.pdf
Immunity Article
Maternal-Derived Hepatitis B Virus e Antigen
Alters Macrophage Function in Offspring to Drive
Viral Persistence after Vertical Transmission
Yongjun Tian,1,2 Cheng-fu Kuo,1,2 Omid Akbari,1and Jing-hsiung James Ou1,*
1Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles,
CA 90033, USA
2Co-first author
*Correspondence:
[email protected]
http://dx.doi.org/10.1016/j.immuni.2016.04.008
母源乙型肝炎病毒e抗原
改变后代的巨噬细胞功能
垂直传播后的病毒持久性
田永军1,2,郭成福1,2 Omid Akbari 1,景雄James Ou1,*
1南加州大学凯克医学院分子微生物学与免疫学系,洛杉矶,
CA 90033,USA
2Co-第一作者
*对应:
[email protected]
In Brief
Children born to mothers who carry HBV
often become chronic HBV carriers. By
developing a mouse model to study this
vertical transmission, Ou and colleagues
find that maternal HBV e antigen
conditions macrophages of the offspring
to suppress the CTL response to HBV,
resulting in HBV persistence in the
offspring.
简单来说
携带HBV的母亲所生的孩子
往往成为慢性HBV携带者。 通过
开发一个鼠标模型来研究这一点
垂直传播,欧和同事
发现母亲HBV e抗原
为后代的巨噬细胞提供条件
抑制CTL对HBV的应答,
导致HBV持久存在于
后代。
Highlights
Developed a mouse model to study effect of maternal HBV on
persistence in offspring
The CTL response to HBV is impaired in the offspring of HBV-
positive mothers
Depletion of macrophages in offspring restores the CTL
response for HBV clearance
Maternal HBeAg enhances PD-L1 expression in
macrophages of offspring to suppress CTL
强调
开发了一个小鼠模型来研究母体HBV对小鼠的影响
坚持后代
HBV的CTL应答在HBV的后代中受损,
积极的母亲
子代巨噬细胞的消耗恢复了CTL
对HBV清除的反应
母体HBeAg增强PD-L1表达
后代巨噬细胞抑制CTL
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