Triggering receptor expressed on myeloid cell-like transcript 2 (TLT-2) is a counter-receptor for B7-H3 and enhances T cell responses

被引：188

作者：

Hashiguchi, Masaaki ^{[1
]}

Kobori, Hiroko ^{[1
]}

Ritprajak, Patcharee ^{[1
]}

Kamimura, Yosuke ^{[1
]}

Kozono, Haruo ^{[2
]}

Azuma, Miyuki ^{[1
]}

机构：

[1] Tokyo Med & Dent Univ, Dept Mol Immunol, Grad Sch, Bunkyo Ku, Tokyo 1138549, Japan

[2] Tokyo Univ Sci, Div Biosignaling, Res Inst Biol Sci, Chiba 2780022, Japan

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2008年 / 105卷 / 30期

关键词：

allergy; cosignal; CD8; T cell activation; contact hypersensitivity;

D O I：

10.1073/pnas.0802423105

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

The B7 family member B7-H3 (CD276) plays important roles in immune responses. However, the function of B7-H3 remains controversial. We found that murine B7-H3 specifically bound to Triggering receptor expressed on myeloid cells (TREM)-like transcript 2 (TLT-2, TREML2). TLT-2 was expressed on CD8(+) T cells constitutively and on activated CD4(+) T cells. Stimulation with B7-H3 transfectants preferentially up-regulated the proliferation and IFN-gamma production of CD8(+) T cells. Transduction of TLT-2 into T cells resulted in enhanced IL-2 and IFN-gamma production via interactions with B7-H3. Blockade of the B7-H3:TLT-2 pathway with a mAb against B7-H3 or TLT-2 efficiently inhibited contact hypersensitivity responses. Our results demonstrate a direct interaction between B7-H3 and TLT-2 that preferentially enhances CD8(+) T cell activation.

引用

页码：10495 / 10500

页数：6

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