Department of Chemistry and Chemical Biology, Cornell University, Ithaca, NY 14853, USA.
Sci Signal. 2013 May 7;6(274):jc2. doi: 10.1126/scisignal.2004061.
Immune defenses depend on the ability of immunoreceptors to recognize foreign antigens and initiate intracellular signaling when a pathogen is detected. Signal initiation requires spatial reorganization of proteins and site-specific receptor phosphorylation, which leads to engagement of feedback loops. This Journal Club discusses recent work using combined experimental and computational approaches to investigate these processes in B cell antigen receptor (BCR) signaling. Specifically, the roles of different kinases in the presence and absence of BCR clustering were evaluated. Results indicated that spleen tyrosine kinase (SYK) can compensate for loss of Src-family kinase activity when receptors are spatially clustered, in part because receptor clustering enables SYK to trigger a positive feedback loop. This study and its implications suggest additional uses for computational models in studies of immunoreceptor signaling and highlight areas where extensions of current methodology are needed to better understand the complexities of biomolecular interactions.
免疫防御依赖于免疫受体识别外来抗原的能力,以及在检测到病原体时启动细胞内信号的能力。信号的启动需要蛋白质的空间重排和受体的特异性磷酸化,这导致了反馈回路的参与。本期期刊俱乐部讨论了最近使用结合实验和计算方法来研究 B 细胞抗原受体 (BCR) 信号转导这些过程的工作。具体来说,评估了不同激酶在 BCR 聚类存在和不存在的情况下的作用。结果表明,当受体空间聚类时,脾酪氨酸激酶 (SYK) 可以弥补 Src 家族激酶活性的丧失,部分原因是受体聚类使 SYK 能够触发正反馈环。这项研究及其意义表明,计算模型在免疫受体信号转导研究中有更多的应用,并强调了需要扩展当前方法来更好地理解生物分子相互作用的复杂性的领域。