Cutting edge: cardiac myosin activates innate immune responses through TLRs.
Cutting edge: cardiac myosin activates innate immune responses through TLRs.
复制标题
DOI：
10.4049/jimmunol.0800861
复制
发表时间：
2009-07-01
期刊：
影响因子：
--
通讯作者：
Cunningham MW
中科院分区：
文献类型：
--
作者：
Zhang P;Cox CJ;Alvarez KM;Cunningham MW
Autoimmune attack on the heart is linked to host immune responses against cardiac myosin, the most abundant protein in the heart. Although adaptive immunity is required for disease, little is known about innate immune mechanisms. Here we report that human cardiac myosin (HCM) acted as an endogenous ligand to directly stimulate human toll-like receptors (TLR) 2 and 8 and activated human monocytes to release proinflammatory cytokines. In addition, pathogenic epitopes of HCM, S2-fragment peptides S2–16 and S2–28, stimulated TLRs directly and activated human monocytes. Our data suggest that cardiac myosin and its pathogenic T cell epitopes may link innate and adaptive immunity in a novel mechanism which could promote chronic inflammation in the myocardium.
登录
查看更多内容
影响因子：
37.8
作者：
Eriksson, U;Kurrer, MO;Kopf, M
通讯作者：
Kopf, M
影响因子：
37.8
作者：
Marty, RR;Dirnhofer, S;Eriksson, U
通讯作者：
Eriksson, U
影响因子：
20.1
作者：
Kubota, T;McTiernan, CF;Feldman, AM
通讯作者：
Feldman, AM
影响因子：
4.4
作者：
Li, Y;Heuser, JS;Cunningham, MW
通讯作者：
Cunningham, MW
影响因子：
56.9
作者：
KRISHER, K;CUNNINGHAM, MW
通讯作者：
CUNNINGHAM, MW