Mouse CD4+ CD25+ T regulatory cells are protected from autologous complement mediated injury by Crry and CD59.
Mouse CD4+ CD25+ T regulatory cells are protected from autologous complement mediated injury by Crry and CD59.
复制标题
Crry 和 CD59 保护小鼠 CD4 CD25 T 调节细胞免受自体补体介导的损伤。
DOI:
10.1016/j.bbrc.2009.03.025
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发表时间:
2009-04-24
影响因子:
3.1
通讯作者:
Lin, Feng
中科院分区:
文献类型:
--
作者:
Li, Qing;Nacion, Kristine;Bu, Hong;Lin, Feng
Self cells depend on surface complement regulators to protect them from autologous complement-mediated attack. CD4+CD25+foxp3+ T regulatory (Treg) cells are critical in maintaining immune homeostasis, however, which complement regulators are expressed on them and how they are protected from autologous complement attack remains unknown. We report here that mouse Treg cells express virtually no DAF or CR1. Instead, all of them express Crry and approximately half of them express CD59. Both Crry-/- and CD59-/- Treg cells exhibit greater complement mediated injury than WT Treg cells. These results clarify the status of cell surface complement regulators on mouse Treg cells and indicate that both Crry and CD59 are required to protect Treg cells from autologous complement-mediated injury. Additionally, these data also argue that different from previous assumption, at least in mice, CD4+CD25+foxp3+ Treg cells are not homogenous and could be further divided into subgroups based on CD59 expression.
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DOI:
10.1084/jem.181.1.151
发表时间:
1995-01-01
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Kim YU;Kinoshita T;Molina H;Hourcade D;Seya T;Wagner LM;Holers VM
通讯作者:
Holers VM
DOI:
10.1084/jem.20041967
发表时间:
2005-05-16
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Heeger PS;Lalli PN;Lin F;Valujskikh A;Liu J;Muqim N;Xu Y;Medof ME
通讯作者:
Medof ME
影响因子:
15.3
作者:
ZALMAN, LS;WOOD, LM;MULLEREBERHARD, HJ
通讯作者:
MULLEREBERHARD, HJ
DOI:
10.1084/jem.168.5.1699
发表时间:
1988-11-01
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Klickstein LB;Bartow TJ;Miletic V;Rabson LD;Smith JA;Fearon DT
通讯作者:
Fearon DT
影响因子:
6.4
作者:
Lin, F;Fukuoka, Y;Medof, ME
通讯作者:
Medof, ME