Enhanced responses of glycosylphosphatidylinositol anchor-deficient T lymphocytes

被引：9

作者：

Hazenbos, WLW

Murakami, Y

Nishimura, J

Takeda, J

Kinoshita, T

机构：

[1] Osaka Univ, Res Inst Microbial Dis, Dept Immunoregulat, Suita, Osaka 5650871, Japan

[2] Duke Univ, Ctr Med, Div Med Oncol & Transplantat, Durham, NC USA

[3] Osaka Univ, Sch Med, Dept Social & Environm Med, Osaka, Japan

来源：

JOURNAL OF IMMUNOLOGY | 2004年 / 173卷 / 06期

关键词：

D O I：

10.4049/jimmunol.173.6.3810

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 functions of GPI-anchored proteins in T lymphocyte activation have been controversial. This issue was addressed by studying the responses of T lymphocytes from T lymphocyte-specific GPI anchor-deficient mice to different stimuli that normally allow coligation of TCR and GPI-anchored proteins. Stimulation of GPI anchor-deficient T lymphocytes with ConA induced 2-fold higher proliferative responses than did normal cells. In response to allogeneic stimulation, proliferation of GPI anchor-deficient T lymphocytes was enhanced 2- to 3-fold. The response to ConA of a GPI anchor-deficient anti-OVA T lymphocyte clone generated from these mice was similar to3-fold higher than that of cells from the same clone in which GPI anchor expression was restored by retroviral transduction. The response of the GPI anchor-deficient cloned anti-OVA T lymphocytes to antigenic stimulation was similar to that of the retrovirally restored cells. These results indicate that coligation with GPI-anchored proteins counteracts the response to TCR stimulation by ConA or alloantigen but not protein Ag.

引用

页码：3810 / 3815

页数：6

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