Peyer's patch is the essential site in initiating murine acute and lethal graft-versus-host reaction

被引：232

作者：

Murai, M

Yoneyama, H

Ezaki, T

Suematsu, M

Terashima, Y

Harada, A

Hamada, H

Asakura, H

Ishikawa, H

Matsushima, K ^{[1
]}

机构：

[1] Univ Tokyo, Dept Mol Prevent Med, Grad Sch Med, Bunkyo Ku, Tokyo 1130033, Japan

[2] Niigata Univ, Dept Internal Med, Sch Med, Niigata 9518122, Japan

[3] Tokyo Womens Med Univ, Dept Anat & Dev Biol, Sch Med, Shinjyuku Ku, Tokyo 1628666, Japan

[4] Keio Univ, Dept Biochem, Sch Med, Shinjyuku Ku, Tokyo 1608582, Japan

[5] Keio Univ, Dept Microbiol, Sch Med, Shinjyuku Ku, Tokyo 1608582, Japan

来源：

NATURE IMMUNOLOGY | 2003年 / 4卷 / 02期

基金：

日本学术振兴会;

关键词：

D O I：

10.1038/ni879

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Acute graft-versus-host disease (a-GVHD) is initiated primarily by immunologically competent cytotoxic T cells (CTLs) that express anti-host specificities. However, the host lymphoid compartment in which these precursor CTLs are initially stimulated remains unclear. Here we show that gut Peyer's patches (PPs) are required to activate anti-host CTL responses in a well characterized murine acute graft-versus-host reaction (a-GVHR) model, involving transfer of parent lymphocytes into F1 hybrid recipients. The a-GVHR was prevented when recruitment of donor T cells into PP was interrupted either by disrupting the gene encoding chemokine receptor CCR5 or by blocking integrin alpha(4)beta(7)-MAdCAM- 1 (mucosal vascular addressin) interactions. Mice deficient for PPs failed to develop a-GVHD in two models of disease induction. Thus, blockade of CTL generation in PPs might offer new strategies for circumventing a-GVHD.

引用

页码：154 / 160

页数：7

共 49 条

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