Cutting edge: Immune stimulation by neisserial porins is toll-like receptor 2 and MyD88 dependent

被引:227
作者
Massari, P
Henneke, P
Ho, Y
Latz, E
Golenbock, DT
Wetzler, LM
机构
[1] Boston Univ, Sch Med, Dept Med, Div Infect Dis, Boston, MA 02118 USA
[2] Univ Massachusetts, Sch Med, Dept Med, Div Infect Dis, Worcester, MA 01665 USA
[3] Free Univ Berlin, Dept Pediat, D-1000 Berlin, Germany
关键词
D O I
10.4049/jimmunol.168.4.1533
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The immunopotentiating activity of neisserial porins, the major outer membrane protein of the pathogenic Neisseria, is mediated by its ability to stimulate B cells and up-regulate the surface expression of B7-2. This ability is dependent on MyD88 and Toll-like receptor (TLR)2 expression, as demonstrated by a lack of a response by B cells from MyD88 or TLR2 knockout mice to the porins. Using previously described TLR2-dependent reporter constructs, these results were confirmed and were shown to be due to induction of NF-kappaB nuclear translocation. This is the first demonstration of known vaccine adjuvant to stimulate immune cells via TLR2.
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收藏
页码:1533 / 1537
页数:5
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