Inhibitory and stimulatory functions of paired Ig-like receptor (PIR) family in RBL-2H3 cells.

Inhibitory and stimulatory functions of paired Ig-like receptor (PIR) family in RBL-2H3 cells.
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RBL-2H3 细胞中配对 Ig 样受体 (PIR) 家族的抑制和刺激功能。

DOI:
--
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发表时间:
1998
影响因子:
4.4
通讯作者:
T. Takai
T. Takai
中科院分区:
医学2区
文献类型:
--
作者:
Y. Yamashita;M. Ono;T. Takai

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在这项研究中,我们利用在大鼠嗜碱性白血病细胞系RBL-2H3上表达的嵌合受体,证明了小鼠杀伤细胞抑制受体样分子、配对的igg样受体(PIRs)或p91的有效调节功能。其中一个嵌合体将PIR-B的跨膜和细胞质结构域融合到IIB型IgG受体的细胞外部分,能够抑制I型受体在共聚集时的ige介导的脱粒反应。这种嵌合体在细胞外培养基中存在和不存在钙离子时也抑制了细胞质Ca2+的动员。PIR-B第三和第四个免疫受体酪氨酸抑制基序样序列的酪氨酸到苯丙氨酸点突变减弱了对脱粒和胞质Ca2+动员的抑制作用,表明这些酪氨酸在传递负信号中起重要作用。相反,由IgG细胞外部分IIB型受体和PIR-A的跨膜和短胞质序列组成的另一种嵌合受体的交联引起Ca2+的动员和脱粒。这些结果表明,PIR分子可以积极和消极地调节细胞功能。
In this study, we demonstrate potent regulatory function of the murine killer cell inhibitory receptor-like molecules, paired Ig-like receptors (PIRs) or p91, using chimeric receptors expressed on the rat basophilic leukemia cell line RBL-2H3. One of the chimeras, which has the transmembrane and cytoplasmic domain of PIR-B fused to the extracellular portion of type IIB receptor for IgG, was able to inhibit the type I receptor for IgE-mediated degranulation response upon coaggregation. This chimera also suppressed cytoplasmic Ca2+ mobilization in the presence and absence of calcium ion in the extracellular medium. Tyrosine to phenylalanine point mutations at the third and fourth immunoreceptor tyrosine-based inhibitory motif-like sequences of PIR-B attenuated the inhibitory effects on degranulation and on cytoplasmic Ca2+ mobilization, indicating the important role of these tyrosines for the delivery of negative signal. In contrast, the cross-linking of another chimeric receptor composed of the type IIB receptor for IgG extracellular portion and the transmembrane and short cytoplasmic sequence of PIR-A elicited Ca2+ mobilization and degranulation. These results indicate that PIR molecules may regulate cellular functions both positively and negatively.
一种新认识的对肥大细胞依赖性超敏反应和炎症进行负调节的途径,该途径由 gp49 家族的内源性细胞表面受体介导。
DOI: --
发表时间: 1997
期刊: Journal of immunology (Baltimore, Md. : 1950)
影响因子: --
作者:
Katz,HR;Austen,KF
通讯作者: Austen,KF
DOI: 10.4049/jimmunol.145.6.1851
发表时间: 1990-09
影响因子: 4.4
作者:
Y. Fukuoka;T. Hugli
通讯作者: Y. Fukuoka;T. Hugli
DOI: 10.1073/pnas.94.10.5261
发表时间: 1997-05-13
影响因子: 11.1
作者:
Kubagawa, H;Burrows, PD;Coopers, MD
通讯作者: Coopers, MD