Nagy Noémi, Mattsson Karin, Maeda Akihiko, Liu Anquan, Székely László, Klein Eva
Microbiology and Tumorbiology Center (MTC), Karolinska Institute, Stockholm, Sweden.
Immunol Lett. 2002 Jun 3;82(1-2):141-7. doi: 10.1016/s0165-2478(02)00029-9.
The unique manifestation of the inherited immunodeficiency, X-linked lymphoproliferative disease (XLP), is the impaired control of EBV infection. The gene, which carries mutations or is deleted in the patients, has been identified (Xq25). The encoded protein (SAP, 128 aa) contains a single SH2 domain and binds to signaling lymphocytic activation molecule (SLAM) and to other related surface molecules that are expressed on activated T, B and NK cells. SAP modifies signal transduction through its association with these molecules. Initially it was assumed that SAP acts passively by interfering and blocking active interactions involving other SH2 carrying molecules. We demonstrated that SAP protein is expressed in activated T and NK, but not in activated B cells. This finding is in line with the fact that in vitro performance of effector cells derived from XLP patients is impaired. However, it is still not known why the severe symptoms (fatal mononucleosis or malignant lymphoproliferation in the survivors of the primary infection) are elicited by EBV. We studied SAP expression in several Burkitt lymphoma (BL) derived lines. In contrast to normal B cells, certain lines expressed SAP. These were all type I cells in the Burkitt line nomenclature: they expressed only one of the EBV encoded proteins (EBNA-1) and their phenotype corresponded to resting B cells. Lymphoblastoid cell lines and type III BLs, whose phenotype resembled activated B cells and expressed all nine EBV encoded proteins, were devoid of SAP. The relationship between cell activation and SAP expression is reciprocal in T and B cells i.e. BL lines, activated T and NK cells express SAP, while BL blasts do not express SAP. This opposite relationship may be exploited for studies about the function of SAP.
遗传性免疫缺陷疾病——X连锁淋巴增殖性疾病(XLP)的独特表现是对EBV感染的控制受损。已鉴定出患者体内携带突变或缺失的基因(Xq25)。编码的蛋白质(SAP,128个氨基酸)含有一个单一的SH2结构域,可与信号淋巴细胞激活分子(SLAM)以及在活化的T、B和NK细胞上表达的其他相关表面分子结合。SAP通过与这些分子的结合来修饰信号转导。最初人们认为,SAP通过干扰和阻断涉及其他携带SH2分子的活性相互作用而被动发挥作用。我们证明,SAP蛋白在活化的T细胞和NK细胞中表达,但在活化的B细胞中不表达。这一发现与XLP患者来源的效应细胞的体外功能受损这一事实相符。然而,目前仍不清楚为什么EBV会引发严重症状(原发性感染幸存者中出现致命性单核细胞增多症或恶性淋巴增殖)。我们研究了几种伯基特淋巴瘤(BL)来源细胞系中的SAP表达。与正常B细胞不同,某些细胞系表达SAP。这些细胞系在伯基特细胞系命名法中均为I型细胞:它们仅表达一种EBV编码蛋白(EBNA-1),其表型与静止B细胞相对应。淋巴母细胞系和III型BLs,其表型类似于活化B细胞并表达所有九种EBV编码蛋白,不表达SAP。在T细胞和B细胞中,细胞活化与SAP表达之间的关系是相互的,即BL细胞系、活化的T细胞和NK细胞表达SAP,而BL母细胞不表达SAP。这种相反的关系可用于研究SAP的功能。