The gene defective in X-linked lymphoproliferative disease controls T cell dependent immune surveillance against Epstein-Barr virus

被引：35

作者：

Howie, D ^{[1
]}

Sayos, J ^{[1
]}

Terhorst, C ^{[1
]}

Morra, M ^{[1
]}

机构：

[1] Harvard Univ, Beth Israel Hosp, Sch Med, Div Immunol, Boston, MA 02215 USA

来源：

CURRENT OPINION IN IMMUNOLOGY | 2000年 / 12卷 / 04期

关键词：

D O I：

10.1016/S0952-7915(00)00123-0

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Our understanding of the X-linked lymphoproliferative syndrome (XLP) has advanced significantly in the past two years. The gene that is aberrant in the condition SH2D1A/SAP, which encodes SAP (signaling lymphocytic activation molecule [SLAM]-associated protein) - was cloned, the crystal structure of its product was solved and insights into the signaling mechanisms of this small SH2-domain-containing protein via the cell surface receptors SLAM and 2B4 have been provided. SAP mutation, and not Epstein-Barr virus infection per se, may be critical for XLP.

引用

页码：474 / 478

页数：5

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