Induction of autophagy by B cell antigen receptor stimulation and its inhibition by costimulation.
Induction of autophagy by B cell antigen receptor stimulation and its inhibition by costimulation.
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DOI：
10.1016/j.bbrc.2008.07.013
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发表时间：
2008-09
影响因子：
3.1
通讯作者：
Kozo Watanabe;S. Ichinose;Koji Hayashizaki;T. Tsubata
中科院分区：
文献类型：
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作者：
Kozo Watanabe;S. Ichinose;Koji Hayashizaki;T. Tsubata
自噬是细胞质成分降解的主要途径，主要是在细胞凋亡被阻断的情况下由一些凋亡刺激物诱导的癌细胞。 B 细胞抗原受体 (BCR) 的连接可诱导细胞凋亡，并在自我耐受中发挥至关重要的作用。然而，BCR 连接是否诱导自噬尚不清楚。在这里，我们证明，在 BCR 连接诱导的细胞凋亡的诱导下，无论细胞凋亡是否被 Bcl-2 的过表达所阻断，自噬体在正常小鼠 B 细胞以及 WEHI-231 B 细胞系中广泛形成。相反，仅用培养基培养的脾B细胞或不发生凋亡的BCR连接的BAL17细胞在凋亡过程中不形成自噬体。此外，当 CD40 信号传导消除凋亡 BCR 信号传导时，不会诱导自噬。这些结果表明，即使在未操作的正常 B 细胞中，自噬也是由凋亡 BCR 信号传导特异性诱导的。
Autophagy is a major pathway for degradation of cytoplasmic components, and is induced by some apoptotic stimuli mostly in cancer cells under the condition in which apoptosis is blocked. Ligation of the B cell antigen receptor (BCR) induces apoptosis and plays a crucial role in self-tolerance. However, whether BCR ligation induces autophagy is not clear. Here, we demonstrate that autophagosomes are extensively formed in normal mouse B cells as well as the WEHI-231 B cell line upon induction of BCR ligation-induced apoptosis regardless of whether apoptosis is blocked by overexpression of Bcl-2. In contrast, autophagosomes were not formed during apoptosis of spleen B cells cultured with medium alone or in BCR-ligated BAL17 cells which do not undergo apoptosis. Moreover, autophagy is not induced when apoptotic BCR signaling is abrogated by CD40 signaling. These results indicate that autophagy is induced specifically by apoptotic BCR signaling even in unmanipulated normal B cells.