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

来源：

JOURNAL OF IMMUNOLOGY | 2002年 / 168卷 / 04期

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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