Molecular mechnisms of immune tolerance.

Nishikawa小组使用血清非依赖的Pro-B细胞培养方法，发现Fyn激酶在融合线的形成中起着重要作用。此外，该研究小组还将Flk2的表达作为定义Pro-B细胞最未分化阶段的标志。除了证明分化的胸腺细胞(c-kit、CD44、CD25-)可以分为FCR和FCR-组外，Katsura小组还表明T细胞系细胞确实是FCR。SuGamura组培育出IL-2受体伽马链突变小鼠。伽马链突变小鼠表现出严重的免疫缺陷，这是由于B和T系细胞减少，完全缺乏NK细胞。平野组证明JAK-STAT通路参与了IL-6受体介导的信号转导。此外，该小组还证明了STAT3在IL-6介导的巨噬细胞分裂中的关键作用。Saito小组利用CD3缺陷小鼠和TCR-TG小鼠杂交建立的小鼠系，展示了TCR信号强度和T细胞选择之间的关系。此外，他们还证明了JAK3在T细胞增殖中的重要性。除了证明p52在/VpreB/B细胞信号转导中的重要性外，Sakaguchi小组还解决了这个新发现的分子的结构。SUDA组报告了胎脾细胞中Fas的强烈表达，以及脂多糖刺激后B细胞上功能性Fas的表达，从而证实了Fas在活化B细胞死亡中的作用。此外，该小组还证明，由于膜结合的人Fas配体的蛋白质降解，Fas可以在保持其细胞溶解活性的同时分泌出来。此外，该小组还开发了针对Fas配体的单克隆，并建立了Fas配体表达的ELISA法。

Using a serum independent pro-B cell cultivation method, the Nishikawa group discovered the important role of fyn kinase in the formation of the (fusion line). In addition, this group showed the use of Flk2 expression as a marker for definition of the most undifferentiated stage of pro-B cells. Along with demonstrating that differentiated thymic cells (c-kit+, CD44+, CD25-) can be divided into FcR+ and FcR- groups, the Katsura group showed that T cell lineage cells are definitively FcR+. The Sugamura group developed IL-2 receptor gamma chain mutant mice. The gamma chain mutant mice showed severe immunodeficiency due to a reduction in B and T lineage cells and a complete lack of NK cells. The Hirano group, demonstrated the participation of the JAK-STAT transduction pathway in IL-6 receptor-mediated signal transduction. In addition, this group demonstrated the critical role of STAT3 in IL-6 mediated macrophage cell division. The Saito group, using a mouse line developed by crossing a CD3 deficient mouse and a TCR-Tg mouse, demonstrated the relationship between TCR signal strength and T cell selection. Also, they demonstrated the importance of Jak3 in T cell proliferation. In addition to demonstrating the importance of p52 in /VpreB/ signal transduction in B cells, the Sakaguchi group also solved the structure of this newly discovered molecule. The Suda group reported the strong expression of FAS in fetal spleen cells as well as the expression of functional FAS on B cells due to LPS stimulation, thus demonstrating the role of Fas in the death of activated B cells. Also, this group demonstrated that, due to protein degradation of membrane-bound human Fas ligand, Fas can be secreted while maintaining its cytotolytic activity. Furthermore, the group developed a monoclonal specific for Fas ligand and established an ELISA assay for Fas ligand expression.