Sato S, Tuscano J M, Inaoki M, Tedder T F
Department of Dermatology, Kanazawa University School of Medicine, Ishikawa, Japan.
Semin Immunol. 1998 Aug;10(4):287-97. doi: 10.1006/smim.1998.0121.
The CD22 cell-surface adhesion molecule is capable of modulating B lymphocyte antigen receptor (BCR)-mediated signals, as well as the generation of BCR-independent signals. Within the cytoplasmic domain of CD22 are motifs that are structurally homologous to known activation and inhibitory motifs. These motifs demonstrate physiologic significance via associations with known effector proteins that likely mediate their corresponding inhibitory and activation roles. Furthermore, the targeted deletion of CD22 in mice results in phenotypic changes and alterations in BCR-mediated signal transduction that are consistent with both positive and negative roles for CD22 in B cell development and activation.
CD22细胞表面黏附分子能够调节B淋巴细胞抗原受体(BCR)介导的信号,以及非BCR依赖性信号的产生。在CD22的胞质结构域内存在与已知激活基序和抑制基序结构同源的基序。这些基序通过与可能介导其相应抑制和激活作用的已知效应蛋白结合而显示出生理意义。此外,在小鼠中靶向缺失CD22会导致表型变化以及BCR介导的信号转导改变,这与CD22在B细胞发育和激活中的正负作用均相符。