Controlling the Toll road to dendritic cell polarization

被引：181

作者：

Mazzoni, A ^{[1
]}

Segal, DM ^{[1
]}

机构：

[1] NCI, Expt Immunol Branch, Bethesda, MD 20892 USA

来源：

JOURNAL OF LEUKOCYTE BIOLOGY | 2004年 / 75卷 / 05期

关键词：

Toll-like receptors; innate immunity; cytokines; infection;

D O I：

10.1189/jlb.1003482

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The activation of dendritic cells (DC) via Toll-like receptors (TLRs) plays a decisive role in shaping the outcome of primary immune responses. Following TLR engagement by microbial products, DC migrate from peripheral tissues to lymphoid organs and up-regulate major histocompatibility complex and costimulatory molecules, acquiring the unique capacity to prime pathogen-specific, naive T cells. In addition, DC determine the character of the ensuing immune response by secreting cytokines that drive the development of T cells into T helper cell type 1 (Th1), Th2, or T regulatory effector cells. Three major factors influence the pattern of cytokines released by DC and accordingly, the Th balance: the lineage to which DC belong; the maturation stimulus; and inflammatory mediators present at the site of infection. A major focus of this review is the capacity of DC to integrate these factors and elicit distinct classes of immune responses.

引用

页码：721 / 730

页数：10

共 128 条

[61]

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[62] Poly(dI•dC)-induced toll-like receptor 3 (TLR3)-mediated activation of NFκB and MAP kinase is through an interleukin-1 receptor-associated kinase (IRAK)-independent pathway employing the signaling components TLR3-TRAF6-TAK1-TAB2-PKR [J].