Signaling and ligand interaction of ILT7: receptor-mediated regulatory mechanisms for plasmacytoid dendritic cells

被引：78

作者：

Cao, Wei ^{[1
]}

Bover, Laura ^{[1
]}

机构：

[1] Univ Texas MD Anderson Canc Ctr, Dept Immunol, Houston, TX 77054 USA

来源：

IMMUNOLOGICAL REVIEWS | 2010年 / 234卷

关键词：

dendritic cells; plasmacytoid dendritic cells; ILT7; BST2; dendritic cell receptors; receptor signal; TOLL-LIKE RECEPTORS; MHC CLASS-I; INTERFERON-PRODUCING CELLS; INHIBITS TLR9-MEDIATED ACTIVATION; IFN-ALPHA PRODUCTION; SINGLE-STRANDED RNA; CUTTING EDGE; T-CELLS; NKG2D RECEPTOR; ANTIGEN PRESENTATION;

D O I：

10.1111/j.0105-2896.2009.00867.x

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Plasmacytoid dendritic cells (pDCs) are specialized dendritic cells (DCs) that produce large amounts of type I interferon (IFN) after Toll-like receptor (TLR) activation. Human pDCs preferentially express immunoglobulin-like transcript 7 (ILT7; LILRA4), which couples with a signaling adapter to activate a prominent immunoreceptor tyrosine-based activation motif (ITAM)-mediated signaling pathway. ILT7 protein directly binds to and can be activated by bone marrow stromal cell antigen 2 (BST2; CD317) protein, the expression of which is found on cells pre-exposed to IFN or on the surface of human cancer cells. The interaction between ILT7 and BST2 functions to assure an appropriate TLR response by pDCs during viral infection and likely participates in pDC-tumor crosstalk. Two opposing modes of receptor-mediated regulatory mechanisms work jointly to fine tune the innate immunity of pDCs.

引用

页码：163 / 176

页数：14

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